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  • 251.
    Saremi, Amin
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Teknisk audiologi. Linköpings universitet, Hälsouniversitetet.
    Stenfelt, Stefan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Teknisk audiologi. Linköpings universitet, Hälsouniversitetet.
    The effect of aging on cochlear amplifier: A simulation approach using a physiologically-based electro-mechanical model of the cochlea2012Inngår i: Canadian Acoustics, ISSN 0711-6659, E-ISSN 2291-1391, Vol. 40, nr 3, s. 128-129Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The electrical, acoustical, and mechanical elements of the cochlea are explicitly integrated into a transmission-line model to develop a physiological interpretation of the human cochlea insofar. The model enables fundamental simulation of specific cochlear lesions such as metabolic presbyacusis. A sound pressure field in the air is transmitted via the outer and middle ear to the inner ear. It causes the stapes to vibrate resulting in a traveling wave along the organ of Corti propagating from base towards apex. As the endocochlear potential (EP) decreases, the MET produces less receptor current which, eventually leading to a decline in the force/displacement generated by the somatic motor. The CFs of the curves tend to move backwards in a presbyacusis cochlea, this result is consistent with Robles and Ruggem where in a passive cochlea, the CFs are shifted backwards.

  • 252.
    Schank, Jesse R.
    et al.
    National Institute on Alcohol Abuse and Alcoholism, NIH; Bethesda, MD, USA.
    Goldstein, Andrea L.
    National Institute on Alcohol Abuse and Alcoholism, NIH; Bethesda, MD, USA.
    Rowe, Kelly E.
    National Institute on Alcohol Abuse and Alcoholism, NIH; Bethesda, MD, USA.
    King, Courtney E.
    National Institute on Alcohol Abuse and Alcoholism, NIH; Bethesda, MD, USA.
    Marusich, Julie A.
    Research Triangle Institute, Research Triangle Park, NC, USA.
    Wiley, Jenny L.
    Research Triangle Institute, Research Triangle Park, NC, USA.
    Carroll, F. Ivy
    Research Triangle Institute, Research Triangle Park, NC, USA.
    Thorsell, Annika
    National Institute on Alcohol Abuse and Alcoholism, NIH; Bethesda, MD, USA.
    Heilig, Markus
    National Institute on Alcohol Abuse and Alcoholism, NIH; Bethesda, MD, USA.
    The kappa opioid receptor antagonist JDTic attenuates alcohol seeking and withdrawal anxiety2012Inngår i: Addiction Biology, ISSN 1355-6215, E-ISSN 1369-1600, Vol. 17, nr 3, s. 634-647Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The role of kappa-opioid receptors (KOR) in the regulation of alcohol-related behaviors is not completely understood. For example, alcohol consumption has been reported to increase following treatment with KOR antagonists in rats, but was decreased in mice with genetic deletion of KOR. Recent studies have further suggested that KOR antagonists may selectively decrease alcohol self-administration in rats following a history of dependence. We assessed the effects of the KOR antagonist JDTic on alcohol self-administration, reinstatement of alcohol seeking induced by alcohol-associated cues or stress, and acute alcohol withdrawal-induced anxiety ('hangover anxiety'). JDTic dose-dependently reversed hangover anxiety when given 48 hours prior to testing, a time interval corresponding to the previously demonstrated anxiolytic efficacy of this drug. In contrast, JDTic decreased alcohol self-administration and cue-induced reinstatement of alcohol seeking when administered 2 hours prior to testing, but not at longer pre-treatment times. For comparison, we determined that the prototypical KOR antagonist nor-binaltorphimine can suppress self-administration of alcohol at 2 hours pre-treatment time, mimicking our observations with JDTic. The effects of JDTic were behaviorally specific, as it had no effect on stress-induced reinstatement of alcohol seeking, self-administration of sucrose, or locomotor activity. Further, we demonstrate that at a 2 hours pre-treatment time JDTic antagonized the antinociceptive effects of the KOR agonist U50,488H but had no effect on morphine-induced behaviors. Our results provide additional evidence for the involvement of KOR in regulation of alcohol-related behaviors and provide support for KOR antagonists, including JDTic, to be evaluated as medications for alcoholism.

  • 253.
    Schank, Jesse R.
    et al.
    National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD, USA.
    Pickens, Charles L.
    National Institute on Drug Abuse, NIH, Bethesda, MD, USA.
    Rowe, Kelly E.
    National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD, USA.
    Cheng, Kejun
    National Institute on Drug Abuse, NIH, Bethesda, MD, USA.
    Thorsell, Annika
    National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD, USA.
    Rice, Kenner C.
    National Institute on Drug Abuse, NIH, Bethesda, MD, USA.
    Shaham, Yavin
    National Institute on Drug Abuse, NIH, Bethesda, MD, USA.
    Heilig, Markus
    National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD, USA.
    Stress-induced reinstatement of alcohol-seeking in rats is selectively suppressed by the neurokinin 1 (NK1) antagonist L8224292011Inngår i: Psychopharmacology, ISSN 0033-3158, E-ISSN 1432-2072, Vol. 218, nr 1, s. 111-119Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    RATIONALE: Genetic inactivation or pharmacological antagonism of neurokinin 1 (NK1) receptors blocks morphine and alcohol reward in rodents, while NK1 antagonism decreases alcohol craving in humans. The role of the NK1 system for relapse-like behavior has not previously been examined.

    OBJECTIVE: Divergence between human and rodent NK1 receptors has limited the utility of NK1 antagonists developed for the human receptor species for preclinical studies of addiction-related behaviors in rats. Here we used L822429, an NK1 antagonist specifically engineered to bind at high affinity to the rat receptor, to assess the effects of NK1 receptor antagonism on alcohol-seeking behaviors in rats.

    METHODS: L822429 (15 and 30 mg/kg) was used to examine effects of NK1 receptor antagonism on operant self-administration of 10% alcohol in 30-min daily sessions, as well as intermittent footshock stress- and cue-induced reinstatement of alcohol-seeking after extinction of lever responding.

    RESULTS: At the doses used, L822429 did not significantly affect alcohol self-administration or cue-induced reinstatement, but potently and dose dependently suppressed stress-induced reinstatement of alcohol seeking, with an essentially complete suppression at the highest dose. The effect of L822429 on stress-induced reinstatement was behaviorally specific. The drug had no effect on conditioned suppression of operant responding following fear conditioning, locomotor activity, or self-administration of a sucrose solution.

    CONCLUSIONS: To the degree that the reinstatement model provides a model of drug relapse, the results provide support for NK1 antagonism as a promising mechanism for pharmacotherapy of alcoholism, acting through suppression of stress-induced craving and relapse.

  • 254.
    Schwieler, Lilly
    et al.
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Larsson, Markus K
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Skogh, Elisabeth
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Hälsouniversitetet. Region Östergötland, Närsjukvården i centrala Östergötland, Psykiatriska kliniken.
    Kegel, Magdalena E
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Orhan, Funda
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Abdelmoaty, Sally
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Finn, Anja
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Bhat, Maria
    AstraZeneca, Research & Development, Innovative Medicines, Personalised Healthcare & Biomarkers, Science for Life Laboratory, Solna, Sweden / Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Samuelsson, Martin
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Närsjukvården i centrala Östergötland, Psykiatriska kliniken.
    Lundberg, Kristina
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten.
    Dahl, Marja-Liisa
    Department of Laboratory Medicine, Division of Clinical Pharmacology, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.
    Sellgren, Carl
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Schuppe-Koistinen, Ina
    AstraZeneca, Research & Development, Innovative Medicines, Personalised Healthcare & Biomarkers, Science for Life Laboratory, Solna, Sweden / Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Svensson, Camilla
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Erhardt, Sophie
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Engberg, Göran
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Increased levels of IL-6 in the cerebrospinal fluid of patients with chronic schizophrenia - significance for activation of the kynurenine pathway.2015Inngår i: Journal of Psychiatry & Neuroscience, ISSN 1180-4882, E-ISSN 1488-2434, Vol. 40, nr 2, s. 126-13Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Accumulating evidence indicates that schizophrenia is associated with brain immune activation. While a number of reports suggest increased cytokine levels in patients with schizophrenia, many of these studies have been limited by their focus on peripheral cytokines or confounded by various antipsychotic treatments. Here, well-characterized patients with schizophrenia, all receiving olanzapine treatment, and healthy volunteers were analyzed with regard to cerebrospinal fluid (CSF) levels of cytokines. We correlated the CSF cytokine levels to previously analyzed metabolites of the kynurenine (KYN) pathway.

    METHODS: We analyzed the CSF from patients and controls using electrochemiluminescence detection with regard to cytokines. Cell culture media from human cortical astrocytes were analyzed for KYN and kynurenic acid (KYNA) using high-pressure liquid chromatography or liquid chromatography/mass spectrometry.

    RESULTS: We included 23 patients and 37 controls in our study. Patients with schizophrenia had increased CSF levels of interleukin (IL)-6 compared with healthy volunteers. In patients, we also observed a positive correlation between IL-6 and the tryptophan:KYNA ratio, indicating that IL-6 activates the KYN pathway. In line with this, application of IL-6 to cultured human astrocytes increased cell medium concentration of KYNA.

    LIMITATIONS: The CSF samples had been frozen and thawed twice before analysis of cytokines. Median age differed between patients and controls. When appropriate, all present analyses were adjusted for age.

    CONCLUSION: We have shown that IL-6, KYN and KYNA are elevated in patients with chronic schizophrenia, strengthening the idea of brain immune activation in patients with this disease. Our concurrent cell culture and clinical findings suggest that IL-6 induces the KYN pathway, leading to increased production of the N-methyl-D-aspartate receptor antagonist KYNA in patients with schizophrenia.

    Fulltekst (pdf)
    fulltext
  • 255.
    Seki, Soju
    et al.
    Univ Calif Los Angeles, CA 90095 USA.
    Yamamoto, Toru
    Univ Calif Los Angeles, CA 90095 USA.
    Quinn, Kiara
    Univ Calif Los Angeles, CA 90095 USA.
    Spigelman, Igor
    Univ Calif Los Angeles, CA 90095 USA; Univ Calif Los Angeles, CA 90095 USA.
    Pantazis, Antonios
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelning för neurobiologi. Linköpings universitet, Medicinska fakulteten. Univ Calif Los Angeles, CA 90095 USA.
    Olcese, Riccardo
    Univ Calif Los Angeles, CA 90095 USA.
    Wiedau-Pazos, Martina
    Univ Calif Los Angeles, CA 90095 USA.
    Chandler, Scott H.
    Univ Calif Los Angeles, CA 90095 USA.
    Venugopal, Sharmila
    Univ Calif Los Angeles, CA 90095 USA.
    Circuit-Specific Early Impairment of Proprioceptive Sensory Neurons in the SOD1(G93A) Mouse Model for ALS2019Inngår i: Journal of Neuroscience, ISSN 0270-6474, E-ISSN 1529-2401, Vol. 39, nr 44, s. 8798-8815Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease in which motor neurons degenerate, resulting in muscle atrophy, paralysis, and fatality. Studies using mouse models of ALS indicate a protracted period of disease development with progressive motor neuron pathology, evident as early as embryonic and postnatal stages. Key missing information includes concomitant alterations in the sensorimotor circuit essential for normal development and function of the neuromuscular system. Leveraging unique brainstem circuitry, we show in vitro evidence for reflex circuit-specific postnatal abnormalities in the jaw proprioceptive sensory neurons in the well-studied SOD1(G)(93A) mouse. These include impaired and arrhythmic action potential burst discharge associated with a deficit in Nav 1.6 Na+ channels. However, the mechanoreceptive and nociceptive trigeminal ganglion neurons and the visual sensory retinal ganglion neurons were resistant to excitability changes in age-matched SOD1(G)(93A )mice. Computational modeling of the observed disruption in sensory patterns predicted asynchronous self-sustained motor neuron discharge suggestive of imminent reflexive defects, such as muscle fasciculations in ALS. These results demonstrate a novel reflex circuit-specific proprioceptive sensory abnormality in ALS.

  • 256.
    Sekijima, Yoshiki
    et al.
    Shinshu University,Matsumoto, Japan.
    Campos, Raul Ivan
    Linköpings universitet, Institutionen för fysik, kemi och biologi, Kemi. Linköpings universitet, Tekniska fakulteten.
    Hammarström, Per
    Linköpings universitet, Institutionen för fysik, kemi och biologi, Kemi. Linköpings universitet, Tekniska fakulteten.
    Nilsson, Peter
    Linköpings universitet, Institutionen för fysik, kemi och biologi, Kemi. Linköpings universitet, Tekniska fakulteten.
    Yoshinaga, Tsuneaki
    Shinshu University, Matsumoto, Japan.
    Nagamatsu, Kiyoshiro
    Shinshu University, Matsumoto, Japan.
    Yazaki, Masahide
    Shinshu University,Matsumoto, Japan.
    Kametani, Fuyuki
    Tokyo Metropolitan Org Medical Research, Japan.
    Ikeda, Shu-ichi
    Shinshu University, Matsumoto, Japan.
    Pathological, biochemical, and biophysical characteristics of the transthyretin variant Y114H (p.Y134H) explain its very mild clinical phenotype2015Inngår i: Journal of the peripheral nervous system, ISSN 1085-9489, E-ISSN 1529-8027, Vol. 20, nr 4, s. 372-379Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Transthyretin (TTR) is a homotetrameric protein that must misfold in order to form amyloid fibrils. Misfolding includes rate limiting tetramer dissociation, followed by fast tertiary structural changes of the monomer that enable aggregation. Hereditary ATTR amyloidosis is an autosomal dominant genetic disorder with systemic deposition of amyloid fibrils induced by TTR gene mutation. We identified a rare Y114H (p.Y134H) TTR variant in a Japanese patient presenting with late-onset, very mild clinical course. The patient had an extremely low serum variant TTR concentration (18% of total TTR), whereas the composition of variant TTR was 55% in amyloid fibrils in tenosynovial tissues obtained at carpal tunnel release surgery. The amyloid fibril deposits in the ATTR Y114H patient had an altered structure compared with that in wild-type ATTR patients, as determined by luminescent conjugated poly/oligo-thiophene fluorescence spectroscopy. Biophysical studies using recombinant protein showed that Y114H TTR was markedly destabilized both thermodynamically and kinetically and was highly amyloidogenic in vitro. These data suggest that extremely low serum variant Y114H TTR concentration, probably due to endoplasmic reticulum-associated degradation of unstable variant TTR protein, protected this patient from severe amyloidosis, as self-assembly of the amyloidogenic intermediate is a concentration-dependent process.

  • 257.
    Shahnawaz, Mohammad
    et al.
    Univ Texas Houston, TX 77004 USA.
    Mukherjee, Abhisek
    Univ Texas Houston, TX 77004 USA.
    Pritzkow, Sandra
    Univ Texas Houston, TX 77004 USA.
    Mendez, Nicolas
    Univ Texas Houston, TX 77004 USA.
    Rabadia, Prakruti
    Univ Texas Houston, TX 77004 USA.
    Liu, Xiangan
    Univ Texas Houston, TX USA.
    Hu, Bo
    Univ Texas Houston, TX USA.
    Schmeichel, Ann
    Mayo Clin, MN USA.
    Singer, Wolfgang
    Mayo Clin, MN USA.
    Wu, Gang
    Univ Texas Houston, TX USA.
    Tsai, Ah-Lim
    Univ Texas Houston, TX USA.
    Shirani, Hamid
    Linköpings universitet, Institutionen för fysik, kemi och biologi, Kemi. Linköpings universitet, Tekniska fakulteten.
    Nilsson, Peter
    Linköpings universitet, Institutionen för fysik, kemi och biologi, Kemi. Linköpings universitet, Tekniska fakulteten.
    Low, Phillip A.
    Mayo Clin, MN USA.
    Soto, Claudio
    Univ Texas Houston, TX 77004 USA.
    Discriminating alpha-synuclein strains in Parkinsons disease and multiple system atrophy2020Inngår i: Nature, ISSN 0028-0836, E-ISSN 1476-4687Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Synucleinopathies are neurodegenerative diseases that are associated with the misfolding and aggregation of alpha-synuclein, including Parkinsons disease, dementia with Lewy bodies and multiple system atrophy(1). Clinically, it is challenging to differentiate Parkinsons disease and multiple system atrophy, especially at the early stages of disease(2). Aggregates of alpha-synuclein in distinct synucleinopathies have been proposed to represent different conformational strains of alpha-synuclein that can self-propagate and spread from cell to cell(3-6). Protein misfolding cyclic amplification (PMCA) is a technique that has previously been used to detect alpha-synuclein aggregates in samples of cerebrospinal fluid with high sensitivity and specificity(7,8). Here we show that the alpha-synuclein-PMCA assay can discriminate between samples of cerebrospinal fluid from patients diagnosed with Parkinsons disease and samples from patients with multiple system atrophy, with an overall sensitivity of 95.4%. We used a combination of biochemical, biophysical and biological methods to analyse the product of alpha-synuclein-PMCA, and found that the characteristics of the alpha-synuclein aggregates in the cerebrospinal fluid could be used to readily distinguish between Parkinsons disease and multiple system atrophy. We also found that the properties of aggregates that were amplified from the cerebrospinal fluid were similar to those of aggregates that were amplified from the brain. These findings suggest that alpha-synuclein aggregates that are associated with Parkinsons disease and multiple system atrophy correspond to different conformational strains of alpha-synuclein, which can be amplified and detected by alpha-synuclein-PMCA. Our results may help to improve our understanding of the mechanism of alpha-synuclein misfolding and the structures of the aggregates that are implicated in different synucleinopathies, and may also enable the development of a biochemical assay to discriminate between Parkinsons disease and multiple system atrophy. Protein misfolding cyclic amplification (PMCA) technology can discriminate between patients with Parkinsons disease and patients with multiple system atrophy on the basis of the characteristics of the alpha-synuclein aggregates in the cerebrospinal fluid.

  • 258.
    Shahul Hameed, L.
    et al.
    Karolinska Institute, Sweden.
    Berg, Daniel A.
    Karolinska Institute, Sweden.
    Belnoue, Laure
    Karolinska Institute, Sweden.
    Jensen, Lasse
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för kardiovaskulär medicin. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Diagnostikcentrum, Klinisk farmakologi. Karolinska Institute, Sweden.
    Cao, Yihai
    Linköpings universitet, Institutionen för medicin och hälsa. Linköpings universitet, Medicinska fakulteten. Karolinska Institute, Sweden; University of Leicester, England.
    Simon, Andras
    Karolinska Institute, Sweden.
    Environmental changes in oxygen tension reveal ROS-dependent neurogenesis and regeneration in the adult newt brain2015Inngår i: eLIFE, E-ISSN 2050-084X, ELIFE SCIENCES PUBLICATIONS LTD, SHERATON HOUSE, CASTLE PARK, CAMBRIDGE, CB3 0AX, ENGLAND, ISSN 2050-084X, Vol. 4, nr e08422Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Organisms need to adapt to the ecological constraints in their habitat. How specific processes reflect such adaptations are difficult to model experimentally. We tested whether environmental shifts in oxygen tension lead to events in the adult newt brain that share features with processes occurring during neuronal regeneration under normoxia. By experimental simulation of varying oxygen concentrations, we show that hypoxia followed by re-oxygenation lead to neuronal death and hallmarks of an injury response, including activation of neural stem cells ultimately leading to neurogenesis. Neural stem cells accumulate reactive oxygen species (ROS) during re-oxygenation and inhibition of ROS biosynthesis counteracts their proliferation as well as neurogenesis. Importantly, regeneration of dopamine neurons under normoxia also depends on ROS-production. These data demonstrate a role for ROS-production in neurogenesis in newts and suggest that this role may have been recruited to the capacity to replace lost neurons in the brain of an adult vertebrate.

    Fulltekst (pdf)
    fulltext
  • 259.
    Shionoya, Kiseko
    et al.
    Centre Européen des Sciences du Goût, CNRS UMR 5170, 15 rue Hugues Picardet, 21000 DIJON, France.
    Datiche, Frédérique
    Centre Européen des Sciences du Goût, CNRS UMR 5170, 15 rue Hugues Picardet, 21000 DIJON, France.
    Inactivation of the basolateral amygdala impairs the retrieval of recent and remote taste-potentiated odor aversion memory2009Inngår i: Neurobiology of Learning and Memory, ISSN 1074-7427, E-ISSN 1095-9564, Vol. 92, nr 4, s. 590-596Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Memory reorganization as a time-dependent process can be investigated using various learning tasks such as the taste-potentiated odor aversion (TPOA). In this paradigm rats acquire a strong aversion to an olfactory cue presented simultaneously with a gustatory cue. Together these cues are paired with a delayed visceral illness. The basolateral amygdaloid nucleus (BLA) plays a key role in TPOA acquisition but its involvement in retrieval remains unclear. We investigated the involvement of the BLA in either recent or remote retrieval of TPOA. In each case, the number of licks observed in response to the presentation of either the odor or the taste was used to assess retrieval. Before the retrieval test, rats received a bilateral infusion of lidocaine to inactivate the BLA. We observed that both recent and remote TPOA retrieval tests induced by the odor presentation were disrupted in the lidocaine-injected rats. By contrast, the BLA inactivation had no effect upon the aversion towards the taste cue regardless of the time of retrieval. The present study provides evidence that BLA functioning is necessary for retrieval of aversive odor memory, even with a long post-acquisition delay.

  • 260.
    Shionoya, Kiseko
    et al.
    Centre de Recherche en Neurosciences de Lyon, INSERM U1028, CNRS UMR5292, University Lyon1, Lyon, France.
    Hegoburu, Chloé
    Centre de Recherche en Neurosciences de Lyon, INSERM U1028, CNRS UMR5292, University Lyon1, Lyon, France.
    Brown, Bruce
    Department of Psychology, Queens College and the Graduate Center, New York, NY, USA.
    Sullivan, Regina
    Child and Adolescent Psychiatry, Emotional Brain Institute, Nathan Kline Institute, New York University School of Medicine, Orangeburg, NY, USA.
    Doyère, Valérie
    Centre de Neurosciences Paris-Sud, University Paris-Sud, UMR 8195, Orsay, France / Centre National de la Recherche Scientifique, Orsay, France.
    Mouly, Anne-Marie
    Centre de Recherche en Neurosciences de Lyon, INSERM U1028, CNRS UMR5292, University Lyon1, Lyon, France.
    It’s time to fear! Interval timing in odor fear conditioning in rats2013Inngår i: Frontiers in Behavioral Neuroscience, ISSN 1662-5153, E-ISSN 1662-5153, Vol. 7, artikkel-id 128Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Time perception is crucial to goal attainment in humans and other animals, and interval timing also guides fundamental animal behaviors. Accumulating evidence has made it clear that in associative learning, temporal relations between events are encoded, and a few studies suggest this temporal learning occurs very rapidly. Most of these studies, however, have used methodologies that do not permit investigating the emergence of this temporal learning. In the present study we monitored respiration, ultrasonic vocalization (USV) and freezing behavior in rats in order to perform fine-grain analysis of fear responses during odor fear conditioning. In this paradigm an initially neutral odor (the conditioned stimulus, CS) predicted the arrival of an aversive unconditioned stimulus (US, footshock) at a fixed 20-s time interval. We first investigated the development of a temporal pattern of responding related to CS-US interval duration. The data showed that during acquisition with odor-shock pairings, a temporal response pattern of respiration rate was observed. Changing the CS-US interval duration from 20-s to 30-s resulted in a shift of the temporal response pattern appropriate to the new duration thus demonstrating that the pattern reflected the learning of the CS-US interval. A temporal pattern was also observed during a retention test 24h later for both respiration and freezing measures, suggesting that the animals had stored the interval duration in long-term memory. We then investigated the role of intra-amygdalar dopaminergic transmission in interval timing. For this purpose, the D1 dopaminergic receptors antagonist SCH23390 was infused in the basolateral amygdala before conditioning. This resulted in an alteration of timing behavior, as reflected in differential temporal patterns between groups observed in a 24h retention test off drug. The present data suggest that D1 receptor dopaminergic transmission within the amygdala is involved in temporal processing.

    Fulltekst (pdf)
    It’s time to fear! Interval timing in odor fear conditioning in rats
  • 261.
    Shionoya, Kiseko
    et al.
    Department of Zoology, University of Oklahoma, Norman, Oklahoma 73019, USA.
    Moriceau, Stephanie
    Department of Zoology, University of Oklahoma, Norman, Oklahoma 73019, USA.
    Lunday, Lauren
    Department of Zoology, University of Oklahoma, Norman, Oklahoma 73019, USA.
    Miner, Cathrine
    Department of Zoology, University of Oklahoma, Norman, Oklahoma 73019, USA.
    Roth, Tania L.
    Department of Zoology, University of Oklahoma, Norman, Oklahoma 73019, USA.
    Sullivan, Regina M.
    Department of Zoology, University of Oklahoma, Norman, Oklahoma 73019, USA.
    Development switch in neural circuitry underlying odor-malaise learning2006Inngår i: Learning & memory (Cold Spring Harbor, N.Y.), ISSN 1072-0502, E-ISSN 1549-5485, Vol. 13, nr 6, s. 801-808Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Fetal and infant rats can learn to avoid odors paired with illness before development of brain areas supporting this learning in adults, suggesting an alternate learning circuit. Here we begin to document the transition from the infant to adult neural circuit underlying odor-malaise avoidance learning using LiCl (0.3 M; 1% of body weight, ip) and a 30-min peppermint-odor exposure. Conditioning groups included: Paired odor-LiCl, Paired odor-LiCl-Nursing, LiCl, and odor-saline. Results showed that Paired LiCl-odor conditioning induced a learned odor aversion in postnatal day (PN) 7, 12, and 23 pups. Odor-LiCl Paired Nursing induced a learned odor preference in PN7 and PN12 pups but blocked learning in PN23 pups. 14C 2-deoxyglucose (2-DG) autoradiography indicated enhanced olfactory bulb activity in PN7 and PN12 pups with odor preference and avoidance learning. The odor aversion in weanling aged (PN23) pups resulted in enhanced amygdala activity in Paired odor-LiCl pups, but not if they were nursing. Thus, the neural circuit supporting malaise-induced aversions changes over development, indicating that similar infant and adult-learned behaviors may have distinct neural circuits.

    Fulltekst (pdf)
    Development switch in neural circuitry underlying odor-malaise learning
  • 262.
    Sikora, Magdalena
    et al.
    Department of Molecular Neuropharmacology, Institute of Pharmacology, Polish Academy of Sciences , 31-343 Krakow, Poland.
    Tokarski, Krzysztof
    Department of Physiology, Institute of Pharmacology, Polish Academy of Sciences , 31-343 Krakow, Poland..
    Bobula, Bartosz
    Department of Physiology, Institute of Pharmacology, Polish Academy of Sciences , 31-343 Krakow, Poland..
    Zajdel, Joanna
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Medicinska fakulteten.
    Jastrzębska, Kamila
    Department of Molecular Neuropharmacology, Institute of Pharmacology, Polish Academy of Sciences , 31-343 Krakow, Poland.
    Cieślak, Przemysław Eligiusz
    Department of Molecular Neuropharmacology, Institute of Pharmacology, Polish Academy of Sciences , 31-343 Krakow, Poland.
    Zygmunt, Magdalena
    Department of Molecular Neuropharmacology, Institute of Pharmacology, Polish Academy of Sciences , 31-343 Krakow, Poland.
    Sowa, Joanna
    Department of Physiology, Institute of Pharmacology, Polish Academy of Sciences , 31-343 Krakow, Poland..
    Smutek, Magdalena
    Department of Molecular Neuropharmacology, Institute of Pharmacology, Polish Academy of Sciences , 31-343 Krakow, Poland.
    Kamińska, Katarzyna
    Department of Pharmacology, Institute of Pharmacology, Polish Academy of Sciences , 31-343 Krakow, Poland.
    Gołembiowska, Krystyna
    Department of Pharmacology, Institute of Pharmacology, Polish Academy of Sciences , 31-343 Krakow, Poland.
    Engblom, David
    Linköpings universitet, Centrum för social och affektiv neurovetenskap (CSAN). Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Medicinska fakulteten.
    Hess, Grzegorz
    Department of Physiology, Institute of Pharmacology, Polish Academy of Sciences , 31-343 Krakow, Poland..
    Przewlocki, Ryszard
    Department of Molecular Neuropharmacology, Institute of Pharmacology, Polish Academy of Sciences, 31-343 Krakow, Poland; Department of Neurobiology and Neuropsychology, Institute of Applied Psychology, Jagiellonian University, 30-348 Krakow, Poland.
    Rodriguez Parkitna, Jan
    Department of Molecular Neuropharmacology, Institute of Pharmacology, Polish Academy of Sciences , 31-343 Krakow, Poland.
    NMDA Receptors on Dopaminoceptive Neurons Are Essential for Drug-Induced Conditioned Place Preference.2016Inngår i: eNeuro, ISSN 2373-2822, Vol. 3, nr 3, artikkel-id ENEURO.0084-15.2016Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Plasticity of the brain's dopamine system plays a crucial role in adaptive behavior by regulating appetitive motivation and the control of reinforcement learning. In this study, we investigated drug- and natural-reward conditioned behaviors in a mouse model in which the NMDA receptor-dependent plasticity of dopaminoceptive neurons was disrupted. We generated a transgenic mouse line with inducible selective inactivation of the NR1 subunit in neurons expressing dopamine D1 receptors (the NR1(D1CreERT2) mice). Whole-cell recordings of spontaneous EPSCs on neurons in the nucleus accumbens confirmed that a population of neurons lacked the NMDA receptor-dependent component of the current. This effect was accompanied by impaired long-term potentiation in the nucleus accumbens and in the CA1 area of the ventral, but not the dorsal, hippocampus. Mutant mice did not differ from control animals when tested for pavlovian or instrumental conditioning. However, NR1(D1CreERT2) mice acquired no preference for a context associated with administration of drugs of abuse. In the conditioned place preference paradigm, mutant mice did not spend more time in the context paired with cocaine, morphine, or ethanol, although these mice acquired a preference for sucrose jelly and an aversion to naloxone injections, as normal. Thus, we observed that the selective inducible ablation of the NMDA receptors specifically blocks drug-associated context memory with no effect on positive reinforcement in general.

    Fulltekst (pdf)
    fulltext
  • 263.
    Simon, Rozalyn
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för radiologiska vetenskaper. Linköpings universitet, Medicinska fakulteten. Linköpings universitet, Centrum för medicinsk bildvetenskap och visualisering, CMIV.
    Pihlsgård, Johan
    Linköpings universitet, Institutionen för medicin och hälsa. Linköpings universitet, Centrum för medicinsk bildvetenskap och visualisering, CMIV. Linköpings universitet, Medicinska fakulteten.
    Berglind, Ulrika
    Linköpings universitet, Institutionen för medicin och hälsa. Linköpings universitet, Medicinska fakulteten.
    Söderfeldt, Birgitta
    Department of Clinical Science and Education, Karolinska Institutet, Stockholm, Sweden.
    Engström, Maria
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för radiologiska vetenskaper. Linköpings universitet, Medicinska fakulteten. Linköpings universitet, Centrum för medicinsk bildvetenskap och visualisering, CMIV.
    Mantra meditation suppression of default mode beyond an active task: a pilot study2017Inngår i: Journal of Cognitive Enhancement, ISSN 2509-3290, Vol. 1, nr 2, s. 219-227Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Within the field of neuroimaging, the discovery of a constellation of brain regions silently active when we are “resting” has provided a new view into the elusive effects of meditative practice. This network, called the default mode network (DMN), has been shown by functional neuroimaging to be active when an individual is at rest. Meta-analyses of the fMRI neurocorrelates of meditation have shown that across diverse practices, the most common general effect appears to be modulation of regions within the DMN. The specific ...

    Fulltekst (pdf)
    fulltext
  • 264.
    Simonoska, Rusana
    et al.
    Karolinska Institutet / Karolinska University Hospital, Stockholm, Sweden.
    Stenberg, Annika E
    Karolinska Institutet / Karolinska University Hospital, Stockholm, Sweden.
    Duan, Maoli
    Karolinska Institutet, Stockholm, Sweden.
    Yakimchuk, Konstantin
    Karolinska Institutet, NOVUM, Huddinge, Sweden.
    Fridberger, Anders
    Karolinska Institutet / Karolinska University Hospital, Stockholm, Sweden.
    Sahlin, Lena
    Karolinska Institutet / Karolinska University Hospital, Stockholm, Sweden.
    Gustafsson, Jan-Åke
    Karolinska Institutet, NOVUM, Huddinge, Sweden.
    Hultcrantz, Malou
    Karolinska Institutet / Karolinska University Hospital, Stockholm, Sweden.
    Inner ear pathology and loss of hearing in estrogen receptor-beta deficient mice2009Inngår i: Journal of Endocrinology, ISSN 1479-6805, Vol. 201, nr 3, s. 397-406Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    There are well known differences between males and females in hearing. In the present study, the role of estrogen receptor-beta (ER-beta; listed as ESR2 in the MGI Database) in hearing was investigated by comparing hearing and morphology of the inner ear in ER-beta knock-out mice (ER-beta(-/-)) with that of wild-type (WT) littermates. Hearing was analyzed with auditory brainstem response audiometry at 3 and 12 months. The ER-beta(-/-) mice were deaf at 1 year of age, and the morphological analysis showed absence of hair cells and loss of the whole organ of Corti initiated in the basal turn of the cochlea. Furthermore, in ER-beta(-/-), but not in WT mice, the spiral ganglion was lacking many of its neurons. Immunostaining showed the presence of both ER-alpha (listed as ESR1 in the MGI Database) and ER-beta in the nuclei of some neurons in the inner ear in WT mice, but no ER-beta was found in the ER-beta(-/-) mice as expected. ER-alpha staining was predominant in the nuclei of large neurons and ER-beta in nuclei of small neurons and fibroblasts. These results reveal that both ERs are present in the inner ear at specific localizations suggesting subtype-specific functions. It is concluded that ER-beta is important for the prevention of age-related hearing loss. These findings strengthen the hypothesis that estrogen has a direct effect on hearing functions.

  • 265.
    Simpson, Elizabeth A
    et al.
    Department of Psychology,University of Miami,Coral Gables, USA.
    Maylott, Sarah E
    Department of Psychology,University of Miami,Coral Gables, USA.
    Heimann, Mikael
    Linköpings universitet, Institutionen för beteendevetenskap och lärande, Psykologi. Linköpings universitet, Filosofiska fakulteten.
    Subiaul, Francys
    Department of Speech and Hearing Science, George Washington University, Washington, USA.
    Paukner, Annika
    Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Dickerson, USA.
    Suomi, Stephen J.
    Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Dickerson, USA.
    Ferrari, Pier F
    Dipartimento di Neuroscienze, Università di Parma, 43123 Parma, Italy; Institut des Sciences Cognitives Marc Jeannerod, CNRS / Université Claude Bernard Lyon, Lyon, France.
    Comments: Animal studies help clarify misunderstandings about neonatal imitation (vol. 40, articelID e400, 2017)2017Inngår i: Behavioral and Brain Sciences, ISSN 0140-525X, E-ISSN 1469-1825, Vol. 40, artikkel-id e400Artikkel i tidsskrift (Annet vitenskapelig)
    Abstract [en]

    Empirical studies are incompatible with the proposal that neonatal imitation is arousal driven or declining with age. Nonhuman primate studies reveal a functioning brain mirror system from birth, developmental continuity in imitation and later sociability, and the malleability of neonatal imitation, shaped by the early environment. A narrow focus on arousal effects and reflexes may grossly underestimate neonatal capacities.

  • 266.
    Singh, Anand Kumar
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Medicinska fakulteten.
    Zajdel, Joanna
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten.
    Mirrasekhian, Elahe
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten.
    Almoosawi, Nader
    Linköpings universitet, Institutionen för klinisk och experimentell medicin. Linköpings universitet, Medicinska fakulteten.
    Frisch, Isabell
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten.
    Klawonn, Anna
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten.
    Jaarola, Maarit
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten.
    Fritz, Michael
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten.
    Engblom, David
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten.
    Prostaglandin-mediated inhibition of serotonin signaling controls the affective component of inflammatory pain2017Inngår i: Journal of Clinical Investigation, ISSN 0021-9738, E-ISSN 1558-8238, Vol. 127, nr 4, s. 1370-1374Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Pain is fundamentally unpleasant and induces a negative affective state. The affective component of pain is mediated by circuits that are distinct from those mediating the sensory-discriminative component. Here, we have investigated the role of prostaglandins in the affective dimension of pain using a rodent pain assay based on conditioned place aversion to formalin injection, an inflammatory noxious stimulus. We found that place aversion induced by inflammatory pain depends on prostaglandin E-2 that is synthesized by cyclooxygenase 2 in neural cells. Further, mice lacking the prostaglandin E-2 receptor EP3 selectively on serotonergic cells or selectively in the area of the dorsal raphe nucleus failed to form an aversion to formalininduced pain, as did mice lacking the serotonin transporter. Chemogenetic manipulations revealed that EP3 receptor activation elicited conditioned place aversion to pain via inhibition of serotonergic neurons. In contrast to their role in inflammatory pain aversion, EP3 receptors on serotonergic cells were dispensable for acute nociceptive behaviors and for aversion induced by thermal pain or a kappa opioid receptor agonist. Collectively, our findings show that prostaglandin-mediated modulation of serotonergic transmission controls the affective component of inflammatory pain.

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    fulltext
  • 267. Bestill onlineKjøp publikasjonen >>
    Skagerlund, Kenny
    Linköpings universitet, Institutionen för beteendevetenskap och lärande, Psykologi. Linköpings universitet, Filosofiska fakulteten.
    Magnitude Processing in Developmental Dyscalculia: A Heterogeneous Learning Disability with Different Cognitive Profiles2016Doktoravhandling, med artikler (Annet vitenskapelig)
    Abstract [en]

    Developmental dyscalculia (DD) is a learning disability that is characterized by severe difficulties with acquiring age-appropriate mathematical skills that cannot be attributed to insufficient education, language skills, or motivation. The prevalence rate is estimated at 3-6%, meaning that a substantial portion of the population struggles to learn mathematics to such a large degree that it affects overall well-being and academic prospects. However, our understanding of the etiology of DD is incomplete and there are competing hypotheses regarding the characteristics of DD and its underlying causal factors. The purpose of the current thesis is to contribute to our understanding of DD from the perspective of cognitive psychology and cognitive neuroscience. To this end, we identify children with DD to identify the cognitive determinants of DD that hamper their ability to learn basic mathematics. It is believed that human beings are endowed with an innate ability to represent numerosities, an ability phylogenetically shared with other species. We investigate whether the purported innate number system plays a role in children with DD insofar as  failures in this system may undermine the acquisition of symbolic representations of number. Although some researchers believe DD is a monolithic learning disability that is genetic and neurobiological in origin, the empirical support for various hypotheses suggests that DD may be shaped by heterogeneous characteristics and underlying causes. The present thesis, and the studies presented therein, provides support for the notion that DD is indeed heterogeneous. We identify at least two subtypes of DD that are characterized by specific deficits in number processing, and one subtype that could more aptly be labelled as a mathematical learning disability, the causal factors of which are likely limited to deficits in non-numerical abilities. In addition, we locate candidate neurocognitive correlates that may be dysfunctional in DD.

    Delarbeid
    1. Development of magnitude processing in children with developmental dyscalculia: space, time, and number
    Åpne denne publikasjonen i ny fane eller vindu >>Development of magnitude processing in children with developmental dyscalculia: space, time, and number
    2014 (engelsk)Inngår i: Frontiers in Psychology, ISSN 1664-1078, E-ISSN 1664-1078, Vol. 5, artikkel-id 675Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    Developmental dyscalculia (DD) is a learning disorder associated with impairments in a preverbal non-symbolic approximate number system (ANS) pertaining to areas in and around the intraparietal sulcus (IPS). The current study sought to enhance our understanding of the developmental trajectory of the ANS and symbolic number processing skills, thereby getting insight into whether a deficit in the ANS precedes or is preceded by impaired symbolic and exact number processing. Recent work has also suggested that humans are endowed with a shared magnitude system (beyond the number domain) in the brain. We therefore investigated whether children with DD demonstrated a general magnitude deficit, stemming from the proposed magnitude system, rather than a specific one limited to numerical quantity. Fourth graders with DD were compared to age-matched controls and a group of ability-matched second graders, on a range of magnitude processing tasks pertaining to space, time, and number. Children with DD displayed difficulties across all magnitude dimensions compared to age-matched peers and showed impaired ANS acuity compared to the younger, ability-matched control group, while exhibiting intact symbolic number processing. We conclude that (1) children with DD suffer from a general magnitude processing deficit, (2) a shared magnitude system likely exists, and (3) a symbolic number-processing deficit in DD tends to be preceded by an ANS deficit.

    sted, utgiver, år, opplag, sider
    Frontiers Research Foundation, 2014
    Emneord
    developmental dyscalculia; number processing; approximate number system; ATOM; time estimation; development
    HSV kategori
    Identifikatorer
    urn:nbn:se:liu:diva-109259 (URN)10.3389/fpsyg.2014.00675 (DOI)000338727700001 ()25018746 (PubMedID)
    Tilgjengelig fra: 2014-08-12 Laget: 2014-08-11 Sist oppdatert: 2017-12-05bibliografisk kontrollert
    2. Number Processing and Heterogeneity of Developmental Dyscalculia: Subtypes With Different Cognitive Profiles and Deficits
    Åpne denne publikasjonen i ny fane eller vindu >>Number Processing and Heterogeneity of Developmental Dyscalculia: Subtypes With Different Cognitive Profiles and Deficits
    2016 (engelsk)Inngår i: Journal of Learning Disabilities, ISSN 0022-2194, E-ISSN 1538-4780, Vol. 49, nr 1, s. 36-50Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    This study investigated if developmental dyscalculia (DD) in children with different profiles of mathematical deficits has the same or different cognitive origins. The defective approximate number system hypothesis and the access deficit hypothesis were tested using two different groups of children with DD (11-13 years old): a group with arithmetic fact dyscalculia (AFD) and a group with general dyscalculia (GD). Several different aspects of number magnitude processing were assessed in these two groups and compared with age-matched typically achieving children. The GD group displayed weaknesses with both symbolic and nonsymbolic number processing, whereas the AFD group displayed problems only with symbolic number processing. These findings provide evidence that the origins of DD in children with different profiles of mathematical problems diverge. Children with GD have impairment in the innate approximate number system, whereas children with AFD suffer from an access deficit. These findings have implications for researchers selection procedures when studying dyscalculia, and also for practitioners in the educational setting.

    sted, utgiver, år, opplag, sider
    SAGE PUBLICATIONS INC, 2016
    Emneord
    developmental dyscalculia; symbolic number processing; nonsymbolic number processing; calculation; arithmetic fact retrieval
    HSV kategori
    Identifikatorer
    urn:nbn:se:liu:diva-124120 (URN)10.1177/0022219414522707 (DOI)000365760200003 ()24598147 (PubMedID)
    Merknad

    Funding Agencies|Swedish Research Council [421-2007-1881]

    Tilgjengelig fra: 2016-01-22 Laget: 2016-01-19 Sist oppdatert: 2018-01-10
    3. Heterogeneity of developmental dyscalculia: Cases with different deficit profiles
    Åpne denne publikasjonen i ny fane eller vindu >>Heterogeneity of developmental dyscalculia: Cases with different deficit profiles
    2017 (engelsk)Inngår i: Frontiers in Psychology, ISSN 1664-1078, E-ISSN 1664-1078Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    Context: The aim was to further understand the heterogeneity of  developmental dyscalculia (DD). Utilizing four children (8-9 year-old) performance was contrasted against predominant hypotheses of DD.

    Case report: Despite showing similar mathematical deficits, these children showed remarkable interindividual variability regarding cognitive profile and deficits. Two cases were consistent with the approximate number system deficit account, and the general magnitude-processing deficit account. One case had an access deficit in combination with a general cognitive deficit. One cases suffered from general cognitive deficits only.

    Conclusions: The results showed that DD cannot be attributed to a single explanatory factor. These findings support a multiple deficits account of DD and suggest that some cases have multiple deficits, whereas other cases have a single deficit. We discuss a previously proposed distinction between primary DD and secondary DD, and suggest hypotheses of dysfunctional neurocognitive correlates responsible for the displayed deficits.

    sted, utgiver, år, opplag, sider
    Frontiers Media, 2017
    Emneord
    Developmental dyscalculia, symbolic number processing, non-symbolic number processing, time processing, spatial processing
    HSV kategori
    Identifikatorer
    urn:nbn:se:liu:diva-124666 (URN)10.3389/fpsyg.2016.02000 (DOI)000391102400001 ()
    Merknad

    Funding agencies: Swedish Research Council for Health, Working Life and Welfare [2008-0238, 2010-0078]

    Tilgjengelig fra: 2016-02-09 Laget: 2016-02-09 Sist oppdatert: 2017-11-30bibliografisk kontrollert
    4. Magnitude processing in the brain: an fMRI study of time, space, and numerosity as a shared cortical system
    Åpne denne publikasjonen i ny fane eller vindu >>Magnitude processing in the brain: an fMRI study of time, space, and numerosity as a shared cortical system
    2016 (engelsk)Inngår i: Frontiers in Human Neuroscience, ISSN 1662-5161, E-ISSN 1662-5161, Vol. 10, nr 500Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    Continuous dimensions, such as time, space, and numerosity, have been suggested to be subserved by common neurocognitive mechanisms. Neuroimaging studies that have investigated either one or two dimensions simultaneously have consistently identified neural correlates in the parietal cortex of the brain. However, the degree of neural overlap across several dimensions has yet to be established, and it remains an open question whether a potential overlap can be conceptualized as a neurocognitive magnitude processing system. The current functional resonance imaging (fMRI) study investigated the potential neurocognitive overlap across three dimensions. A sample of adults (N = 24) performed three different magnitude processing tasks: a temporal discrimination task, a number discrimination task, and a line length discrimination task. A conjunction analysis revealed several overlapping neural substrates across multiple magnitude dimensions, and we argue that these cortical nodes comprise a distributed magnitude processing system. Key components of this predominantly right-lateralized system include the intraparietal sulcus, insula, premotor cortex, inferior frontal gyrus and frontal eye-fields. Together with previous research highlighting IPS, our results suggest that the insula also is a core component of the magnitude processing system. We discuss the functional role of each of these components in the magnitude processing system and suggest that further research of this system may provide insight into the etiology of neurodevelopmental disorders where cognitive deficits in magnitude processing are manifest.

    sted, utgiver, år, opplag, sider
    Frontiers Media, 2016
    Emneord
    Number processing, Time processing, Spatial processing, Magnitude processing, Insula, Intraparietal sulcus (IPS)
    HSV kategori
    Identifikatorer
    urn:nbn:se:liu:diva-124667 (URN)10.3389/fnhum.2016.00500 (DOI)000385888600001 ()27761110 (PubMedID)
    Merknad

    Funding Agencies|Swedish Council for Working Life and Social Research [2010-0078]

    Tilgjengelig fra: 2016-02-09 Laget: 2016-02-09 Sist oppdatert: 2018-01-10bibliografisk kontrollert
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    Download (jpg)
    presentationsbild
  • 268.
    Skagerlund, Kenny
    et al.
    Linköpings universitet, Institutionen för beteendevetenskap och lärande, Psykologi. Linköpings universitet, Filosofiska fakulteten. Univ Miami, FL 33124 USA.
    Bolt, Taylor
    Univ Miami, FL 33124 USA.
    Nomi, Jason S.
    Univ Miami, FL 33124 USA.
    Skagenholt, Mikael
    Linköpings universitet, Institutionen för beteendevetenskap och lärande, Psykologi. Linköpings universitet, Filosofiska fakulteten.
    Västfjäll, Daniel
    Linköpings universitet, Institutionen för beteendevetenskap och lärande, Psykologi. Linköpings universitet, Filosofiska fakulteten. Decis Res, OR USA.
    Träff, Ulf
    Linköpings universitet, Institutionen för beteendevetenskap och lärande, Psykologi. Linköpings universitet, Filosofiska fakulteten.
    Uddin, Lucina Q.
    Univ Miami, FL 33124 USA.
    Disentangling Mathematics from Executive Functions by Investigating Unique Functional Connectivity Patterns Predictive of Mathematics Ability2019Inngår i: Journal of cognitive neuroscience, ISSN 0898-929X, E-ISSN 1530-8898, Vol. 31, nr 4, s. 560-573Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    What are the underlying neurocognitive mechanisms that give rise to mathematical competence? This study investigated the relationship between tests of mathematical ability completed outside the scanner and resting-state functional connectivity (FC) of cytoarchitectonically defined subdivisions of the parietal cortex in adults. These parietal areas are also involved in executive functions (EFs). Therefore, it remains unclear whether there are unique networks for mathematical processing. We investigate the neural networks for mathematical cognition and three measures of EF using resting-state fMRI data collected from 51 healthy adults. Using 10 ROIs in seed to whole-brain voxel-wise analyses, the results showed that arithmetical ability was correlated with FC between the right anterior intraparietal sulcus (hIP1) and the left supramarginal gyrus and between the right posterior intraparietal sulcus (hIP3) and the left middle frontal gyrus and the right premotor cortex. The connection between the posterior portion of the left angular gyrus and the left inferior frontal gyrus was also correlated with mathematical ability. Covariates of EF eliminated connectivity patterns with nodes in inferior frontal gyrus, angular gyrus, and middle frontal gyrus, suggesting neural overlap. Controlling for EF, we found unique connections correlated with mathematical ability between the right hIP1 and the left supramarginal gyrus and between hIP3 bilaterally to premotor cortex bilaterally. This is partly in line with the "mapping hypothesis" of numerical cognition in which the right intraparietal sulcus subserves nonsymbolic number processing and connects to the left parietal cortex, responsible for calculation procedures. We show that FC within this circuitry is a significant predictor of math ability in adulthood.

    Fulltekst (pdf)
    fulltext
  • 269.
    Skinbjerg, Mette
    et al.
    National Institutes of Health, NIH, Bethesda, MD, USA.
    Ariano, Marjorie A.
    The Chicago Medical School at Rosalind Franklin University of Medicine and Science, North Chicago, Illinois, USA.
    Thorsell, Annika
    National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD, USA.
    Heilig, Markus
    National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD, USA.
    Halldin, Christer
    Karolinska Institutet, Stockholm, Sweden.
    Innis, Robert B.
    National Institute of Mental Health, NIH, Bethesda, MD, USA.
    Sibley, David R.
    National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD, USA.
    Arrestin3 mediates D(2) dopamine receptor internalization2009Inngår i: Synapse, ISSN 0887-4476, E-ISSN 1098-2396, Vol. 63, nr 7, s. 621-624Artikkel i tidsskrift (Fagfellevurdert)
  • 270.
    Skinbjerg, Mette
    et al.
    National Institute of Mental Health, Bethesda, MD, USA.
    Liow, Jeih-San
    National Institute of Mental Health, Bethesda, MD, USA.
    Seneca, Nicholas
    National Institute of Mental Health, Bethesda, MD, USA.
    Hong, Jinsoo
    National Institute of Mental Health, Bethesda, MD, USA.
    Lu, Shuiyu
    National Institute of Mental Health, Bethesda, MD, USA.
    Thorsell, Annika
    National Institute on Alcohol Abuse and Alcoholism, NIH; Bethesda, MD, USA.
    Heilig, Markus
    National Institute on Alcohol Abuse and Alcoholism, NIH; Bethesda, MD, USA.
    Pike, Victor W.
    National Institute of Mental Health, Bethesda, MD, USA.
    Halldin, Christer
    Karolinska Institutet, Stockholm, Sweden.
    Sibley, David R.
    National Institute of Neurological Disorders and Stroke, Bethesda, MD, USA.
    Innis, Robert B.
    National Institute of Mental Health, Bethesda, MD, USA.
    D2 dopamine receptor internalization prolongs the decrease of radioligand binding after amphetamine: a PET study in a receptor internalization-deficient mouse model2010Inngår i: NeuroImage, ISSN 1053-8119, E-ISSN 1095-9572, Vol. 50, nr 4, s. 1402-1407Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Dopamine released by amphetamine decreases the in vivo binding of PET radioligands to the dopamine D(2) receptor. Although concentrations of extracellular dopamine largely return to baseline within 1 to 2 h after amphetamine treatment, radioligand binding remains decreased for several hours. The purpose of this study was to determine whether the prolonged decrease of radioligand binding after amphetamine administration is caused by receptor internalization. To distinguish dopamine displacement from receptor internalization, we used wild-type and arrestin3 (arr3) knockout mice, which are incapable of internalizing D(2) receptors. In addition, we used both the D(2) selective agonist [(11)C]MNPA (which is thought to bind to the high affinity state of the receptor) and the D(2) selective antagonist [(18)F]fallypride (which does not differentiate between high and low affinity state). After an initial baseline scan, animals were divided in three groups for a second scan: either 30 min or 4 h after amphetamine administration (3 mg/kg, i.p.) or as retest. At 30 min, [(11)C]MNPA showed greater displacement than [(18)F]fallypride, but each radioligand gave similar displacement in knockout and wild-type mice. At 4 h, the binding of both radioligands returned to baseline in arr3 knockout mice, but remained decreased in wild-type mice. Radioligand binding was unaltered on retest scanning. Our results suggest that the prolonged decrease of radioligand binding after amphetamine is mainly due to internalization of the D(2) receptor rather than dopamine displacement. In addition, this study demonstrates the utility of small animal PET to study receptor trafficking in vivo in genetically modified mice.

  • 271.
    Slawecki, Craig J
    et al.
    The Scripps Research Institute, La Jolla, CA, USA.
    Thorsell, Annika
    The Scripps Research Institute, La Jolla, CA, USA.
    Ehlers, C L
    The Scripps Research Institute, La Jolla, CA, USA.
    Antagonism of neuropeptide YY1 receptors does not inhibit ethanol's effects on cortical EEG and ERPs in Wistar rats2005Inngår i: Journal of Studies on Alcohol, ISSN 0096-882X, E-ISSN 1934-2683, Vol. 66, nr 4, s. 559-566Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVE: Ethanol and neuropeptide Y (NPY) can have additive neurobehavioral effects. In the present study, the NPY Y1 receptor antagonist BIBP3226 was administered alone or in combination with a moderate dose of ethanol to determine whether it interacted with the neurobehavioral effects of ethanol.

    METHOD: Male Wistar rats were implanted with cortical recording electrodes and a lateral ventricular cannula. The effects of 1 nmol BIBP3226, 0.75 g/kg ethanol and the combination (BIBP3226 + EtOH) on neurophysiological activity and locomotion were then assessed.

    RESULTS: Ethanol significantly increased 1-2 Hz parietal cortical power and this effect was partially antagonized by BIBP3226. Peak frequencies in the parietal cortical 6-8 Hz and 8-16 Hz bands were also altered by ethanol, but these effects were not reversed by BIBP3226. BIBP3226 or ethanol, when administered alone, did not alter motor activity or cortical event-related potentials (ERPs) but administration of BIBP3226 + EtOH reduced motor activity, reduced parietal cortical N1 ERP amplitude and increased frontal cortical N1 ERP latency.

    CONCLUSIONS: In the present study, the most prominent effect of antagonizing central NPY Y1 receptors was a facilitation of the effects of ethanol. In particular, the effects of combined administration of BIBP3226 and ethanol are indicative of enhanced sedation and possibly cognitive impairment.

  • 272.
    Slawecki, Craig J.
    et al.
    The Scripps Research Institute, La Jolla, CA, USA.
    Thorsell, Annika K.
    National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD, United States.
    El Khoury, Aram
    Karolinska Institute, Stockholm, Sweden.
    Mathé, Aleksander A
    Karolinska Institute, Stockholm, Sweden.
    Ehlers, Cindy L
    The Scripps Research Institute, La Jolla, CA, USA.
    Increased CRF-like and NPY-like immunoreactivity in adult rats exposed to nicotine during adolescence: relation to anxiety-like and depressive-like behavior2005Inngår i: Neuropeptides, ISSN 0143-4179, E-ISSN 1532-2785, Vol. 39, nr 4, s. 369-377Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVE: Recently, animal models have been developed that demonstrate that adolescent nicotine exposure produces neurobehavioral changes which persist into adulthood. This study further examined the impact of adolescent nicotine exposure on anxiety-like and depressive-like behavior, as well as on levels of corticotropin-releasing factor (CRF) and neuropeptide Y (NPY) in this model.

    METHODS: Male adolescent rats (35-40 days old) were administered nicotine using Nicoderm CQ patches (Smith-Kline Beecham). Behavior in the elevated plus maze (EPM) and forced swim test (FST) was assessed 2-3 weeks after exposure ended. Brain levels of CRF and NPY were then assessed 5-6 weeks after behavioral tests were completed. In addition, blood and brain levels of nicotine resulting from nicotine treatment were examined.

    RESULTS: After 5 days of exposure to 5 mg/kg/day nicotine, blood levels of nicotine averaged 66+/-5 ng/ml and brain nicotine levels averaged 52+/-4 ng/g. Rats exposed to nicotine displayed an anxiety-like profile in the EPM (i.e., decreased time spent in the open arms) and an antidepressant-like profile in the FST (i.e., less time spent immobile). Rats exposed to nicotine also had increased hypothalamic and frontal cortical CRF, increased hypothalamic and hippocampal NPY, and a decreased ratio of NPY to CRF in the amygdala.

    CONCLUSIONS: This study demonstrates that adolescent nicotine exposure produces lasting increases in anxiety-like behavior and may reduce depressive-like behavior. These behavioral changes also occurred in concert with alterations in CRF and NPY systems. Thus, lasting neurobehavioral changes associated with adolescent nicotine exposure may be related to allostatic changes in stress peptide systems.

  • 273.
    Smith, Jonathan J.
    et al.
    Department of Zoology, University of Oklahoma, Norman, OK 73019, USA.
    Shionoya, Kiseko
    Department of Zoology, University of Oklahoma, Norman, OK 73019, USA.
    Sullivan, Regina M.
    Department of Zoology, University of Oklahoma, Norman, OK 73019, USA / Emotional Brain Institute, Nathan Kline Institute for Psychiatric Research, 140 Old Orangeburg Road, Orangeburg, NY 10962, USA / Department of Child and Adolescent Psychiatry, New York University School of Medicine, 577 First Avenue, New York, NY 10016, USA.
    Wilson, Donald A.
    Department of Zoology, University of Oklahoma, Norman, OK 73019, USA / Emotional Brain Institute, Nathan Kline Institute for Psychiatric Research, 140 Old Orangeburg Road, Orangeburg, NY 10962, USA / Department of Child and Adolescent Psychiatry, New York University School of Medicine, 577 First Avenue, New York, NY 10016, USA.
    Auditory Stimulation Dishabituates Olfactory Responses via Noradrenergic Cortical Modulation2009Inngår i: Neural Plasticity, ISSN 2090-5904, E-ISSN 1687-5443, Vol. 2009, artikkel-id 754014Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Dishabituation is a return of a habituated response if context or contingency changes. In the mammalian olfactory system, metabotropic glutamate receptor mediated synaptic depression of cortical afferents underlies short-term habituation to odors. It was hypothesized that a known antagonistic interaction between these receptors and norepinephrine -receptors provides a mechanism for dishabituation. The results demonstrate that a 108 dB siren induces a two-fold increase in norepinephrine content in the piriform cortex. The same auditory stimulus induces dishabituation of odor-evoked heart rate orienting bradycardia responses in awake rats. Finally, blockade of piriform cortical norepinephrine -receptors with bilateral intracortical infusions of propranolol (100  M) disrupts auditory-induced dishabituation of odor-evoked bradycardia responses. These results provide a cortical mechanism for a return of habituated sensory responses following a cross-modal alerting stimulus.

    Fulltekst (pdf)
    Auditory Stimulation Dishabituates Olfactory Responses via Noradrenergic Cortical Modulation
  • 274.
    Stenbäck, Victoria
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten.
    Speech masking speech in everyday communication: The role of inhibitory control and working memory capacity2016Doktoravhandling, med artikler (Annet vitenskapelig)
    Abstract [en]

    Age affects hearing and cognitive abilities. Older people, with and without hearing impairment (HI), exhibit difficulties in hearing speech in noise. Elderly individuals show greater difficulty in segregating target speech from distracting background noise, especially if the noise is competing speech with meaningful contents, so called informational maskers. Working memory capacity (WMC) has proven to be a crucial factor in comprehending speech in noise, especially for people with hearing loss. In auditory scenes where speech is disrupted by competing speech, high WMC has proven to facilitate the ability to segregate target speech and inhibit responses to irrelevant information. People with low WMC are more prone to be disrupted by competing speech and exhibit more difficulties in hearing target speech in complex listening environments. Furthermore, elderly individuals with a HI experience more difficulties in switching attention between wanted and irrelevant stimuli, and they employ more resources and time to attend to the stimuli than do normally - hearing (NH) younger adults.

    This thesis investigated the importance of inhibitory control and WMC for speech recognition in noise, and perceived listening effort. Four studies were conducted. In the first study, the aim was to develop a test of inhibitory control for verbal content, and to investigate the relation between inhibitory control and WMC, and how these two abilities related to speech recognition in noise, in young normally – hearing (YNH) individuals.

    In the second study we aimed to investigate the same relationship as in the first study to further strengthen the validity of the inhibitory test developed, as well as the importance of lexical access. It was also an aim to investigate the influence of age and hearing status on lexical access and WMC, and their respective roles for speech recognition in noise in both YNH and elderly HI (EHI) individuals.

    Study one and two showed that, for YNH, inhibitory control was related to speech recognition in noise, indicating that inhibitory control can help to predict speech recognition in noise performance. The relationship between WMC and speech recognition in noise in YNH shifted in the studies, suggesting that this relationship is multifaceted and varying. Lexical access was of little importance for YNH, although for EHI individuals, both WMC and lexical access was of importance for speech recognition in noise, suggesting that different cognitive abilities were of importance for the YNH and EHI individuals Study three investigated the relationship between inhibitory control, WMC, speech recognition in noise, and perceived listening effort, in YNH and elderly, for their age, NH, individuals (ENH). In study four the same relationships as in study three were investigated, albeit in EHI individuals. Two speech materials with different characteristics, masked with four background noises were used. The results in study three showed that less favourable SNRs were needed for informational maskers than for maskers without semantic content. ENH individuals were more susceptible to informational maskers than YNH individuals. In contrast, in study four, more favourable SNRs were needed for informational maskers. In both studies, results showed that speech recognition in noise performance differed depending on the characteristics of the speech material.

    The studies showed that high WMC, compared to low WMC, was beneficial for speech recognition in noise, especially for informational maskers, and resulted in lower ratings of perceived effort. Varying results were found in study three and four regarding perceived effort and inhibitory control. In study three good inhibitory control was associated with lower effort rating, while in study four, individuals with a HI and good inhibitory control rated effort as higher.

    The results suggest that hearing status, age, and cognitive abilities, contribute to the differences in performance between YNH, ENH, and EHI individuals in speech – recognition – in – noise - and cognitive tasks.

    This thesis has, for the first time, demonstrated that a measure of inhibitory control of verbal content, is related to speech recognition in noise performance in YNH, ENH and EHI individuals. Results presented in this thesis also show that both WMC and inhibitory control are related to an individuals’ perception of how effortful a listening task is. It also adds to the literature that WMC is related to speech recognition in noise performance for ENH and EHI individuals, but that this relationship is not as robust in YNH individuals.

    Delarbeid
    1. The Swedish Hayling task, and its relation to working memory, verbal ability, and speech-recognition-in-noise
    Åpne denne publikasjonen i ny fane eller vindu >>The Swedish Hayling task, and its relation to working memory, verbal ability, and speech-recognition-in-noise
    2015 (engelsk)Inngår i: Scandinavian Journal of Psychology, ISSN 0036-5564, E-ISSN 1467-9450, Vol. 56, nr 3, s. 264-272Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    Cognitive functions and speech-recognition-in-noise were evaluated with a cognitive test battery, assessing response inhibition using the Hayling task, working memory capacity (WMC) and verbal information processing, and an auditory test of speech recognition. The cognitive tests were performed in silence whereas the speech recognition task was presented in noise. Thirty young normally-hearing individuals participated in the study. The aim of the study was to investigate one executive function, response inhibition, and whether it is related to individual working memory capacity (WMC), and how speech-recognition-in-noise relates to WMC and inhibitory control. The results showed a significant difference between initiation and response inhibition, suggesting that the Hayling task taps cognitive activity responsible for executive control. Our findings also suggest that high verbal ability was associated with better performance in the Hayling task. We also present findings suggesting that individuals who perform well on tasks involving response inhibition, and WMC, also perform well on a speech-in-noise task. Our findings indicate that capacity to resist semantic interference can be used to predict performance on speech-in-noise tasks.

    sted, utgiver, år, opplag, sider
    Wiley, 2015
    Emneord
    executive functions, inhibition, cognitive control, working memory capacity, speech recognition in noise, hearing
    HSV kategori
    Identifikatorer
    urn:nbn:se:liu:diva-117054 (URN)10.1111/sjop.12206 (DOI)000354185700003 ()25819210 (PubMedID)
    Prosjekter
    Tal som störning vid språklig kommunikation
    Forskningsfinansiär
    Swedish Research Council, 421-2009-1753
    Tilgjengelig fra: 2015-04-14 Laget: 2015-04-14 Sist oppdatert: 2017-12-04bibliografisk kontrollert
    2. Executive functions and working memory capacity in speech communication under adverse conditions
    Åpne denne publikasjonen i ny fane eller vindu >>Executive functions and working memory capacity in speech communication under adverse conditions
    2016 (engelsk)Inngår i: Speech, Language and Hearing, ISSN 2050-571X, Vol. 19, nr 4, s. 218-226Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    Introduction: Working memory is assumed to play a major part in hearing and communication in everyday listening situations. Our working memory stores information, but in suboptimal listening conditions, interfering stimuli can lead to information only being partially stored, or even missed. Research suggests that a high working memory capacity (WMC) might not just be a result of a large store, but in addition good inhibitory control can facilitate working memory, and therefore aid in situations where focus on a target stimulus while ignoring distractors is needed.

    Objective: The aim of the present study was to investigate how individual WMC, cognitive inhibition, and lexical decision relate to listening to speech under adverse conditions in two separate groups: 46 young normally hearing (NH) and 40 elderly hearing-impaired (HI) individuals.

    Results: It showed that lexical access was of little importance for young NH individuals in a speech-in-noise test, but that high lexical decision-making was associated with lower signal-to-noise ratios for the elderly HI individuals. The results also showed that WMC was of importance for word recognition in a speech-in-noise test for elderly participants, when the 80% word recognition criterion was targeted, but not for the young NH individuals. Finally, results suggest that cognitive inhibition, as measured with the Hayling task, was important for young NH individuals when listening conditions are suboptimal.

    Conclusion: In conclusion, hearing loss is a strong contributing factor to declines in the ability to recognize speech in noise, and in order to assess speech-recognition-in-noise performance, individual differences in WMC and cognitive inhibition should be taken into consideration. Future research should include various age groups, with and without hearing loss, as well as measures of WMC, cognitive inhibition, and lexical access when assessing the ability to listen to speech under adverse conditions.

    sted, utgiver, år, opplag, sider
    Taylor & Francis, 2016
    HSV kategori
    Identifikatorer
    urn:nbn:se:liu:diva-133193 (URN)10.1080/2050571X.2016.1196034 (DOI)
    Tilgjengelig fra: 2016-12-14 Laget: 2016-12-14 Sist oppdatert: 2018-01-13bibliografisk kontrollert
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    Speech masking speech in everyday communication: The role of inhibitory control and working memory capacity
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  • 275.
    Stenbäck, Victoria
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten.
    Hällgren, Mathias
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Sinnescentrum, Öron- näsa- och halskliniken US.
    Larsby, Birgitta
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten.
    Executive functions and working memory capacity in speech communication under adverse conditions2016Inngår i: Speech, Language and Hearing, ISSN 2050-571X, Vol. 19, nr 4, s. 218-226Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Introduction: Working memory is assumed to play a major part in hearing and communication in everyday listening situations. Our working memory stores information, but in suboptimal listening conditions, interfering stimuli can lead to information only being partially stored, or even missed. Research suggests that a high working memory capacity (WMC) might not just be a result of a large store, but in addition good inhibitory control can facilitate working memory, and therefore aid in situations where focus on a target stimulus while ignoring distractors is needed.

    Objective: The aim of the present study was to investigate how individual WMC, cognitive inhibition, and lexical decision relate to listening to speech under adverse conditions in two separate groups: 46 young normally hearing (NH) and 40 elderly hearing-impaired (HI) individuals.

    Results: It showed that lexical access was of little importance for young NH individuals in a speech-in-noise test, but that high lexical decision-making was associated with lower signal-to-noise ratios for the elderly HI individuals. The results also showed that WMC was of importance for word recognition in a speech-in-noise test for elderly participants, when the 80% word recognition criterion was targeted, but not for the young NH individuals. Finally, results suggest that cognitive inhibition, as measured with the Hayling task, was important for young NH individuals when listening conditions are suboptimal.

    Conclusion: In conclusion, hearing loss is a strong contributing factor to declines in the ability to recognize speech in noise, and in order to assess speech-recognition-in-noise performance, individual differences in WMC and cognitive inhibition should be taken into consideration. Future research should include various age groups, with and without hearing loss, as well as measures of WMC, cognitive inhibition, and lexical access when assessing the ability to listen to speech under adverse conditions.

  • 276.
    Stenfelt, Stefan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Teknisk audiologi. Linköpings universitet, Hälsouniversitetet.
    A model for prediction of own voice alteration with hearing aids2012Inngår i: Speech Perception and Auditory Disorders / [ed] T. Dau, M.L. Jepsen, T. Poulsen, J.C. Dalsgaard, Danavox Jubilee Foundation , 2012, s. 323-330Kapittel i bok, del av antologi (Annet vitenskapelig)
  • 277.
    Stenfelt, Stefan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Teknisk audiologi. Linköpings universitet, Hälsouniversitetet.
    Binaural hearing with bone conduction stimulation – what is possible?2013Konferansepaper (Fagfellevurdert)
  • 278.
    Stenfelt, Stefan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Teknisk audiologi. Linköpings universitet, Hälsouniversitetet.
    Bone Conduction and the Middle Ear2012Inngår i: The Middle Ear: Science, Otosurgery, and Technology / [ed] Sunil Puria, Arthur N. Popper, Richard F. Fay, New York: Springer, 2012, s. 135-169Kapittel i bok, del av antologi (Fagfellevurdert)
    Abstract [en]

    With more than a century of research in the field of bone conduction (BC) hearing, the importance of the contributors for bone-conducted sound is not clarified and there is no consensus on the issues. However, the literature suggests that the inner ear fluid inertia is the most important mechanism for speech frequencies. But several other contributors are generally within 10 dB of the most important one, including inertial effect of the middle ear ossicles. Most pathology in the outer and middle ear that severely affects the air conduction sound transmission affects the bone conduction sensitivity only to a minor extent. So even if the changed bone conduction sensitivity in a middle ear lesion is helpful for understanding underlying bone conduction physiology, its clinical relevance is minor. Also, the use of BC thresholds for differential diagnosis of the specific middle ear lesion is risky; the Carhart notch is not always identifiable in cases of otosclerotic ears, and other lesions show BC depression similar to the Carhart notch. There are several pitfalls when conducting BC testing. The most common are occlusion of the ear canal, airborne sound radiation from the transducers, and unmasked or overmasked nontest ear.

  • 279.
    Stenfelt, Stefan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Teknisk audiologi. Linköpings universitet, Hälsouniversitetet.
    Bredbandsmätning av mellanörat2013Inngår i: Audio-Nytt, ISSN 0347-6308, Vol. 40, nr 1-2, s. 24-25Artikkel i tidsskrift (Annet (populærvitenskap, debatt, mm))
  • 280.
    Stenfelt, Stefan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Teknisk audiologi. Linköpings universitet, Hälsouniversitetet.
    Skull vibration during bone conduction hearing2013Inngår i: 20th International Congress on Sound and Vibration, Bangkok, Thailand, 2013Konferansepaper (Fagfellevurdert)
  • 281.
    Stenfelt, Stefan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Teknisk audiologi. Linköpings universitet, Hälsouniversitetet.
    The demands on the cognitive system – what the audiogram does not tell you2013Konferansepaper (Fagfellevurdert)
  • 282.
    Stenfelt, Stefan
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Teknisk audiologi. Linköpings universitet, Hälsouniversitetet.
    Zeitooni, Mehrnaz
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Teknisk audiologi. Linköpings universitet, Hälsouniversitetet.
    Binaural Hearing Ability in Normal Hearing Subjects When Stimulation is by Bone Conduction2012Konferansepaper (Fagfellevurdert)
  • 283.
    Stenfelt, Stefan
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Teknisk audiologi. Linköpings universitet, Hälsouniversitetet.
    Zeitooni, Mehrnaz
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Teknisk audiologi. Linköpings universitet, Hälsouniversitetet.
    Loudness functions with air and bone conduction stimulation in normal-hearing subjects using a categorical loudness scaling procedure2013Inngår i: Hearing Research, ISSN 0378-5955, E-ISSN 1878-5891, Vol. 301, s. 85-92Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    In a previous study (Stenfelt and Håkansson, 2002) a loudness balance test between bone conducted (BC) sound and air conducted (AC) sound was performed at frequencies between 0.25 and 4 kHz and at levels corresponding to 30–80 dB HL. The main outcome of that study was that for maintaining equal loudness, the level increase of sound with BC stimulation was less than that of AC stimulation with a ratio between 0.8 and 0.93 dB/dB. However, because it was shown that AC and BC tone cancellation was independent of the stimulation level, the loudness level difference did not originate in differences in basilar membrane stimulation. Therefore, it was speculated that the result could be due to the loudness estimation procedure. To investigate this further, another loudness estimation method (adaptive categorical loudness scaling) was here employed in 20 normal-hearing subjects.

    The loudness of a low-frequency and a high-frequency noise burst was estimated using the adaptive categorical loudness scaling technique when the stimulation was bilaterally by AC or BC. The sounds where rated on an 11-point scale between inaudible and too loud. The total dynamic range for these sounds was over 80 dB when presented by AC (between inaudible and too loud) and the loudness functions were similar for the low and the high-frequency stimulation. When the stimulation was by BC the loudness functions were steeper and the ratios between the slopes of the AC and BC loudness functions were 0.88 for the low-frequency sound and 0.92 for the high-frequency sound. These results were almost equal to the previous published results using the equal loudness estimation procedure, and it was unlikely that the outcome stems from the loudness estimation procedure itself. One possible mechanism for the result was loudness integration of multi-sensory input. However, no conclusive evidence for such a mechanism could be given by the present study.

    Fulltekst (pdf)
    fulltext
  • 284.
    Stenfelt, Stefan
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Teknisk audiologi. Linköpings universitet, Hälsouniversitetet.
    Zeitooni, Mehrnaz
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Teknisk audiologi. Linköpings universitet, Hälsouniversitetet.
    Loudness Growth with Bone Conduction Stimulation in Normal Hearing Subjects Using a Categorical Scaling Procedure2012Konferansepaper (Fagfellevurdert)
  • 285.
    Stojakovic, Andrea
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Medicinska fakulteten.
    Paz-Filho, Gilberto
    Australian National University, Australia.
    Arcos-Burgos, Mauricio
    Australian National University, Australia.
    Licinio, Julio
    South Australian Health and Medical Research Institute, Australia; Flinders University of South Australia, Australia.
    Wong, Ma-Li
    South Australian Health and Medical Research Institute, Australia; Flinders University of South Australia, Australia.
    Mastronardi, Claudio A.
    Australian National University, Australia; South Australian Health and Medical Research Institute, Australia; Flinders University of South Australia, Australia.
    Role of the IL-1 Pathway in Dopaminergic Neurodegeneration and Decreased Voluntary Movement2017Inngår i: Molecular Neurobiology, ISSN 0893-7648, E-ISSN 1559-1182, Vol. 54, nr 6, s. 4486-4495Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Interleukin-1 (IL-1), a proinflammatory cytokine synthesized and released by activated microglia, can cause dopaminergic neurodegeneration leading to Parkinsons disease (PD). However, it is uncertain whether IL-1 can act directly, or by exacerbating the harmful actions of other brain insults. To ascertain the role of the IL-1 pathway on dopaminergic neurodegeneration and motor skills during aging, we compared mice with impaired [caspase-1 knockout (casp1(-/-))] or overactivated IL-1 activity [IL-1 receptor antagonist knockout (IL-1ra(-/-))] to wild-type (wt) mice at young and middle age. Their motor skills were evaluated by the open-field and rotarod tests, and quantification of their dopamine neurons and activated microglia within the substantia nigra were performed by immunohistochemistry. IL-1ra(-/-) mice showed an age-related decline in motor skills, a reduced number of dopamine neurons, and an increase in activated microglia when compared to wt or casp1(-/-) mice. Casp1(-/-) mice had similar changes in motor skills and dopamine neurons, but fewer activated microglia cells than wt mice. Our results suggest that the overactivated IL-1 pathway occurring in IL-1ra(-/-) mice in the absence of inflammatory interventions (e.g., intracerebral injections performed in animal models of PD) increased activated microglia, decreased the number of dopaminergic neurons, and reduced their motor skills. Decreased IL-1 activity in casp1(-/-) mice did not yield clear protective effects when compared with wt mice. In summary, in the absence of overt brain insults, chronic activation of the IL-1 pathway may promote pathological aspects of PD per se, but its impairment does not appear to yield advantages over wt mice.

    Fulltekst (pdf)
    fulltext
  • 286.
    Stojakovic, Andrea
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Medicinska fakulteten.
    Walczak, Magdalena
    Jagiellonian Univ, Poland.
    Cieslak, Przemyslaw E.
    Polish Acad Sci, Poland.
    Trenk, Aleksandra
    Jagiellonian Univ, Poland.
    Sköld, Johan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten.
    Zajdel, Joanna
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten.
    Mirrasekhian, Elahe
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten.
    Karlsson, Camilla
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten.
    Thorsell, Annika
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten.
    Heilig, Markus
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Närsjukvården i centrala Östergötland, Psykiatriska kliniken.
    Parkitna, Jan Rodriguez
    Polish Acad Sci, Poland.
    Blasiak, Tomasz
    Jagiellonian Univ, Poland.
    Engblom, David
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten.
    Several behavioral traits relevant for alcoholism are controlled by gamma 2 subunit containing GABA(A) receptors on dopamine neurons in mice2018Inngår i: Neuropsychopharmacology, ISSN 0893-133X, E-ISSN 1740-634X, Vol. 43, nr 7, s. 1548-1556Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The risk factors for developing alcohol addiction include impulsivity, high sensitivity to the rewarding action of ethanol, and low sensitivity to its sedative and intoxicating effects. Genetic variation in GABA(A) receptor subunits, including the gamma 2 subunit (Gabrg2), affects the risk for developing alcoholism. Alcohol directly potentiates GABA(A) receptors and activates the mesolimbic dopamine system. Here, we deleted Gabrg2 selectively in dopamine cells of adult mice. The deletion resulted in elevated firing of dopamine neurons and made them less sensitive to drugs acting at GABA(A) receptors. At the behavioral level, the deletion increased exploratory behavior and augmented both correct and incorrect responding in the go/no-go task, a test often used to assay the response inhibition component of impulsivity. In addition, conditioned place preference to alcohol, but not to cocaine or morphine, was increased. Ethanol-induced locomotor activation was enhanced in the mice lacking Gabrg2 on dopaminergic cells, whereas the sedative effect of alcohol was reduced. Finally, the alcohol drinking, but not the alcohol preference, at a high concentration was increased in the mutant mice. In summary, deletion of Gabrg2 on dopamine cells induced several behavioral traits associated with high risk of developing alcoholism. The findings suggest that mice lacking Gabrg2 on dopaminergic cells could be used as models for individuals at high risk for developing alcoholism and that GABA(A) receptors on dopamine cells are protective against the development of excessive alcohol drinking.

  • 287.
    Stokowska, Anna
    et al.
    Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
    Atkins, Alison L
    Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
    Morán, Javier
    Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
    Pekny, Tulen
    Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
    Bulmer, Linda
    Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
    Pascoe, Michaela C
    Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
    Barnum, Scott R
    University of Alabama, Birmingham, Alabama, USA.
    Wetsel, Rick A
    University of Texas-Houston, Houston, Texas, USA.
    Nilsson, Jonas A
    Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
    Dragunow, Mike
    The University of Auckland, Auckland, New Zealand.
    Pekna, Marcela
    Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden, Florey Institute of Neuroscience and Mental Health, Parkville, Victoria, Australia, Hunter Medical Research Institute, University of Newcastle, New South Wales, Australia.
    Complement peptide C3a stimulates neural plasticity after experimental brain ischaemia.2017Inngår i: Brain, ISSN 0006-8950, E-ISSN 1460-2156, Vol. 140, nr 2Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Ischaemic stroke induces endogenous repair processes that include proliferation and differentiation of neural stem cells and extensive rewiring of the remaining neural connections, yet about 50% of stroke survivors live with severe long-term disability. There is an unmet need for drug therapies to improve recovery by promoting brain plasticity in the subacute to chronic phase after ischaemic stroke. We previously showed that complement-derived peptide C3a regulates neural progenitor cell migration and differentiation in vitro and that C3a receptor signalling stimulates neurogenesis in unchallenged adult mice. To determine the role of C3a-C3a receptor signalling in ischaemia-induced neural plasticity, we subjected C3a receptor-deficient mice, GFAP-C3a transgenic mice expressing biologically active C3a in the central nervous system, and their respective wild-type controls to photothrombotic stroke. We found that C3a overexpression increased, whereas C3a receptor deficiency decreased post-stroke expression of GAP43 (P < 0.01), a marker of axonal sprouting and plasticity, in the peri-infarct cortex. To verify the translational potential of these findings, we used a pharmacological approach. Daily intranasal treatment of wild-type mice with C3a beginning 7 days after stroke induction robustly increased synaptic density (P < 0.01) and expression of GAP43 in peri-infarct cortex (P < 0.05). Importantly, the C3a treatment led to faster and more complete recovery of forepaw motor function (P < 0.05). We conclude that C3a-C3a receptor signalling stimulates post-ischaemic neural plasticity and intranasal treatment with C3a receptor agonists is an attractive approach to improve functional recovery after ischaemic brain injury.media-1vid110.1093/brain/aww314_video_abstractaww314_video_abstract.

  • 288. Bestill onlineKjøp publikasjonen >>
    Stratmann, Johannes
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi och molekylär medicin. Linköpings universitet, Medicinska fakulteten.
    Genetic Mechanisms during Terminal Cell Fate Specification in the Drosophila CNS2017Doktoravhandling, med artikler (Annet vitenskapelig)
    Abstract [en]

    Specification of the many unique neuronal subtypes found in the nervous system depends on spatiotemporal cues and terminal selector cascades, mostly acting in sequential combinatorial codes of transcription factors (TFs) to dictate cell fate. Out of 10,000 cells in the Drosophila embryonic ventral nerve cord (VNC), only 28 cells selectively express Nplp1. The Nplp1 neurons in the Drosophila VNC can be subdivided into the thoracic ventro-lateral Tv1 and the dorsal-medial dAp neurons. Nplp1 expression in both cell subtypes is activated by the same terminal selector cascade: col > ap/eya > dimm > Nplp1. However Tv1 and dAp neurons are generated by different neuronal progenitors (neuroblasts, NB), and depend on different upstream cues to activate the cell specification cascade. The Tv1 cells are generated by NB5-6T, and in these cells the Nplp1 terminal selector cascade is triggered by spatio-temporal input provided by Antp/hth/exd/lbe/cas. Our studies identified that NB4-3 gives rise to the dAp cells and that the Nplp1 terminal selector cascade in dAp cells is activated by Kr/pdm>grn. I demonstrated how two different spatio-temporal combinations can funnel on a shared downstream terminal selector cascade to determine a highly related cell fate, in different regions of the VNC. I tested this scenario at the molecular level, by identification of cisregulatory modules (CRMs) for the main factors involved in the Nplp1 terminal selector cascade. Intriguingly, I found that col is under control of two separate CRMs, which are controlled by either Antp/hth/exd/lbe/cas in the NB5-6T lineage, and Kr/pdm/grn in the NB4-3 lineage. In addition, CRISPR deletion of the endogenous col CRMs did not result in loss of Col and Nplp1, indicating that col might be under control of more, yet unidentified CRMs. Nplp1 is expressed in one out of four cells in the thoracic Apterous cluster (Ap cluster); the Tv1 cell. The allocation of the right cell fate to each of the four Ap cluster cells, is regulated by the sub-temporal cascade including the factors Sqz/Nab/Svp, acting downstream of the temporal factor Cas. The sub-temporal factors have a repressive action on Col and Dimm, and thus on the terminal selector cascade regulating Nplp1 expression in the Tv1  cell. We demonstrated that the late and Tv1 specific expression of the early temporal factor Kr suppresses Svp in the Tv1 cell and allows for the progression of the Nplp1 cell fate specification cascade. Hence, early temporal factors involved in temporal progression of neuronal progenitors, can be re-utilized late and postmitotically to specify cell fate. It is tempting to speculate that similar mechanisms act to generate similar cell fate in different regions of the CNS, as well as the issue of sub-temporal multitasking, are common features both in Drosophila and higher organisms.

    Delarbeid
    1. Neuronal Cell Fate Specification by the Convergence of Different Spatiotemporal Cues on a Common Terminal Selector Cascade
    Åpne denne publikasjonen i ny fane eller vindu >>Neuronal Cell Fate Specification by the Convergence of Different Spatiotemporal Cues on a Common Terminal Selector Cascade
    Vise andre…
    2016 (engelsk)Inngår i: PLoS biology, ISSN 1544-9173, E-ISSN 1545-7885, Vol. 14, nr 5, s. e1002450-Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    Specification of the myriad of unique neuronal subtypes found in the nervous system depends upon spatiotemporal cues and terminal selector gene cascades, often acting in sequential combinatorial codes to determine final cell fate. However, a specific neuronal cell subtype can often be generated in different parts of the nervous system and at different stages, indicating that different spatiotemporal cues can converge on the same terminal selectors to thereby generate a similar cell fate. However, the regulatory mechanisms underlying such convergence are poorly understood. The Nplp1 neuropeptide neurons in the Drosophila ventral nerve cord can be subdivided into the thoracic-ventral Tv1 neurons and the dorsal-medial dAp neurons. The activation of Nplp1 in Tv1 and dAp neurons depends upon the same terminal selector cascade: colamp;gt;ap/eyaamp;gt;dimmamp;gt;Nplp1. However, Tv1 and dAp neurons are generated by different neural progenitors (neuroblasts) with different spatiotemporal appearance. Here, we find that the same terminal selector cascade is triggered by Kr/pdmamp;gt;grn in dAp neurons, but by Antp/hth/exd/lbe/cas in Tv1 neurons. Hence, two different spatiotemporal combinations can funnel into a common downstream terminal selector cascade to determine a highly related cell fate.

    sted, utgiver, år, opplag, sider
    PUBLIC LIBRARY SCIENCE, 2016
    HSV kategori
    Identifikatorer
    urn:nbn:se:liu:diva-129501 (URN)10.1371/journal.pbio.1002450 (DOI)000376906100001 ()27276273 (PubMedID)
    Merknad

    Funding Agencies|Swedish Research Council (VR-NT) [621-2010-5214]; Wallenberg Foundation [KAW2012.0101]; Swedish Cancer Foundation [120531]; Spanish Ministerio de Economia y Competitividad [BFU2013-43858-P]

    Tilgjengelig fra: 2016-06-20 Laget: 2016-06-20 Sist oppdatert: 2017-11-28
    2. Neuronal cell fate diversification controlled by sub-temporal action of Kruppel
    Åpne denne publikasjonen i ny fane eller vindu >>Neuronal cell fate diversification controlled by sub-temporal action of Kruppel
    2016 (engelsk)Inngår i: eLIFE, E-ISSN 2050-084X, Vol. 5, artikkel-id e19311e19311Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    During Drosophila embryonic nervous system development, neuroblasts express a programmed cascade of five temporal transcription factors that govern the identity of cells generated at different time-points. However, these five temporal genes fall short of accounting for the many distinct cell types generated in large lineages. Here, we find that the late temporal gene castor sub-divides its large window in neuroblast 5-6 by simultaneously activating two cell fate determination cascades and a sub-temporal regulatory program. The sub-temporal program acts both upon itself and upon the determination cascades to diversify the castor window. Surprisingly, the early temporal gene Kruppel acts as one of the sub-temporal genes within the late castor window. Intriguingly, while the temporal gene castor activates the two determination cascades and the sub-temporal program, spatial cues controlling cell fate in the latter part of the 5-6 lineage exclusively act upon the determination cascades.

    sted, utgiver, år, opplag, sider
    eLife Sciences Publications Ltd., 2016
    HSV kategori
    Identifikatorer
    urn:nbn:se:liu:diva-132850 (URN)10.7554/eLife.19311 (DOI)000386456200001 ()27740908 (PubMedID)
    Merknad

    Funding Agencies|Svenska Forskningsradet Formas [621-2013-5258]; Cancerfonden [120531]; Knut och Alice Wallenbergs Stiftelse [KAW2011.0165]; Ministerio de Industria, Energia y Turismo [BFU2013-43858-P]

    Tilgjengelig fra: 2016-12-06 Laget: 2016-11-30 Sist oppdatert: 2018-03-19
    3. Neuronal cell fate specification by the molecular convergence of different spatio-temporal cues on a common initiator terminal selector gene
    Åpne denne publikasjonen i ny fane eller vindu >>Neuronal cell fate specification by the molecular convergence of different spatio-temporal cues on a common initiator terminal selector gene
    2017 (engelsk)Inngår i: PLoS Genetics, ISSN 1553-7390, E-ISSN 1553-7404, Vol. 13, nr 4, s. 26Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    The extensive genetic regulatory flows underlying specification of different neuronal subtypes are not well understood at the molecular level. The Nplp1 neuropeptide neurons in the developing Drosophila nerve cord belong to two sub-classes; Tv1 and dAp neurons, generated by two distinct progenitors. Nplp1 neurons are specified by spatial cues; the Hox homeotic network and GATA factor grn, and temporal cues; the hb -greater than Kr -greater than Pdm -greater than cas -greater than grh temporal cascade. These spatio-temporal cues combine into two distinct codes; one for Tv1 and one for dAp neurons that activate a common terminal selector feedforward cascade of col -greater than ap/eya -greater than dimm -greater than Nplp1. Here, we molecularly decode the specification of Nplp1 neurons, and find that the cis-regulatory organization of col functions as an integratory node for the different spatio-temporal combinatorial codes. These findings may provide a logical framework for addressing spatio-temporal control of neuronal sub-type specification in other systems. [ABSTRACT FROM AUTHOR]

    sted, utgiver, år, opplag, sider
    PLOS, 2017. s. 26
    Emneord
    Animal cells, Animal models, Animals, Arthropoda, Biochemistry, Biology and life sciences, Cell binding, Cell biology, Cell physiology, Cell staining, Cellular neuroscience, Cellular types, Developmental biology, DNA-binding proteins, Drosophila, Drosophila melanogaster, Embryology, Embryos, Experimental organism systems, Gene expression, Gene regulation, Genetics, Insects, Invertebrates, Model organisms, Neurons, Neuroscience, Organisms, Proteins, Regulatory proteins, Research and analysis methods, Research Article, Specimen preparation and treatment, Staining, Transcription factors
    HSV kategori
    Identifikatorer
    urn:nbn:se:liu:diva-136555 (URN)10.1371/journal.pgen.1006729 (DOI)000402549200037 ()28414802 (PubMedID)
    Merknad

    Funding agencies: Cancerfonden [140780]; Vetenskapsradet [621-20135258]; Knut och Alice Wallenbergs Stiftelse [KAW2011.0165]

    Tilgjengelig fra: 2017-04-19 Laget: 2017-04-19 Sist oppdatert: 2017-06-26bibliografisk kontrollert
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    Genetic Mechanisms during Terminal Cell Fate Specification in the Drosophila CNS
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  • 289. Bestill onlineKjøp publikasjonen >>
    Sundberg, Sofie
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelning för neurobiologi. Linköpings universitet, Medicinska fakulteten.
    Neuromodulation, Short-Term and Long-Term Plasticity in Corticothalamic and Hippocampal Neuronal Networks2018Doktoravhandling, med artikler (Annet vitenskapelig)
    Abstract [en]

    Research in neuroscience relies to a large extent on the use of genetically modified animals. Extensive validation of new and existing models is a requirement for the acquisition of trustworthy data and to enable generalization to human physiology and disease. This thesis includes, as one part (project I and II), validation of a transgenic mouse model with the expression of the enzyme Cre-recombinase restricted to neurons in a band in the deepest layer of the cerebral cortex. Secondly, in project III we use this mouse model to study the process of short-term plasticity in neuronal cultures. Lastly, we investigate synaptic plasticity by studying the effect that the developmental signaling factor Hedgehog (Hh) has on mature hippocampal cultures (project IV). 

    In project I and II, we identified the transgenic mouse Neurotensin receptor 1-Cre GN220 (Ntsr1-Cre) to have Cre expression targeted to the corticothalamic (CT) pyramidal neuron population in neocortical layer 6. Further, we identified a small group of Ntsr1-Cre positive neurons present in the white matter that is distinct from the CT population. We also identified that the transcription factor Forkhead box protein 2 (FoxP2) was specifically expressed by CT neurons in neocortex. In project I, we further explored the sensitivity of CT neurons to cholinergic modulation and found that they are sensitive to even low concentrations of acetylcholine. Both nicotinic and muscarinic acetylcholine receptors depolarize the neurons. Presenting CT neurons as a potential target for cholinergic modulation in wakefulness and arousal. 

    In project III we studied Ntsr1-Cre neurons in cortical cultures and found that cultured neurons have similar properties to CT neurons in the intact nervous system. Ntsr1-Cre neurons in culture often formed synapses with itself, i. e. autapses, with short-term synaptic plasticity that was different to ordinary synapses. By expressing the light-controlled ion channel channelrhodopsin-2 (ChR2) in Ntsr1-Cre neurons we could compare paired pulse ratios with either electrical or light stimulation. Electrical stimulation typically produced paired-pulse facilitation while light stimulation produced paired pulse depression, presumably due to unphysiological Ca2+ influx in presynaptic terminals. Thus, cultured Ntsr1- Cre neurons can be used to study facilitation, and ChR2 could be used as a practical tool to further study the dependence of Ca2+ for short-term plasticity. 

    In project IV we investigated the role of Hedgehog (Hh) for hippocampal neuron plasticity. Non-canonical Hh-signaling negatively regulated NMDA- receptor function through an unknown mechanism resulting in changes in NMDA-receptor mediated currents and subsequent changes in AMPA- receptors in an LTP/LTD manner in mature neurons. Proposing Hh as a slow-acting factor with ability to scale down excitation for instances of excessive activity, e.g. during an epileptic seizure, as a mechanism to make the activity in the neuronal networks stable. 

     

    Delarbeid
    1. Cre-expressing neurons in visual cortex of Ntsr1-Cre GN220 mice are corticothalamic and are depolarized by acetylcholine
    Åpne denne publikasjonen i ny fane eller vindu >>Cre-expressing neurons in visual cortex of Ntsr1-Cre GN220 mice are corticothalamic and are depolarized by acetylcholine
    2018 (engelsk)Inngår i: Journal of Comparative Neurology, ISSN 0021-9967, E-ISSN 1096-9861, Vol. 526, nr 1, s. 120-132Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    The Ntsr1-Cre GN220 mouse expresses Cre-recombinase in corticothalamic (CT) neurons in neocortical layer 6. It is not known if the other major types of pyramidal neurons in this layer also express this enzyme. By electrophysiological recordings in slices and histological analysis of the uptake of retrogradely transported beads we show that Cre-positive neurons are CT and not corticocortical or corticoclaustral types. Furthermore, we show that Ntsr1-Cre-positive cells are immuno-positive for the nuclear transcription factor Forkhead box protein P2 (FoxP2). We conclude that Cre-expression is limited to a specific type of pyramidal neuron: CT. However, it appears as not all CT neurons are Cre-expressing; there are indications that the penetrance of the gene is about 90%. We demonstrate the utility of assigning a specific identity to individual neurons by determining that the CT neurons are potently modulated by acetylcholine acting on both nicotinic and muscarinic acetylcholine receptors. These results corroborate the suggested function of these neurons in regulating the gain of thalamocortical transfer of sensory information depending on attentional demand and state of arousal.

    sted, utgiver, år, opplag, sider
    WILEY, 2018
    Emneord
    acetylcholine; corticothalamic; claustrum; FoxP2; Ntsr1; visual cortex; RRID: MMRRC_030648-UCD; RRID: AB_10000240; RRID: AB_2313516; RRID: AB_2107107; RRID: SCR_002074
    HSV kategori
    Identifikatorer
    urn:nbn:se:liu:diva-144137 (URN)10.1002/cne.24323 (DOI)000418575500008 ()28884467 (PubMedID)
    Merknad

    Funding Agencies|Swedish Research Council [3050, 2862]; Linkoping University

    Tilgjengelig fra: 2018-01-10 Laget: 2018-01-10 Sist oppdatert: 2018-10-12
    2. Cre-expressing neurons in the cortical white matter of Ntsr1-Cre GN220 mice
    Åpne denne publikasjonen i ny fane eller vindu >>Cre-expressing neurons in the cortical white matter of Ntsr1-Cre GN220 mice
    2018 (engelsk)Inngår i: Neuroscience Letters, ISSN 0304-3940, E-ISSN 1872-7972, Vol. 675, s. 36-40Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    Genetically modified mouse strains that express Cre-recombinase in specific neuronal sub-populations have become widely used tools for investigating neuronal function. The Ntsr1-Cre GN220 mouse expresses this enzyme in corticothalamic neurons in layer 6 of cerebral cortex. We observed that about 7% of Cre-expressing cells in the primary visual cortex are found within the white matter bordering layer 6. By using the immunohistochemical marker for layer 6 neurons, Forkhead box protein 2 (FoxP2), and fluorescently conjugated latex beads injected into the dorsal lateral geniculate nucleus, we show that about half of these cells are similar to and could belong to the layer 6 corticothalamic neuron population. The other half seems to be a distinct white matter (WM) neuron sub-population that we estimate to constitute 2-4% of the total cortical Cre expressing population. Staining for the neuronal marker Neuronal nuclei (NeuN) revealed that about 15-40% of WM neurons are Cre-expressing. Thus, the potential contribution from WM neurons needs to be considered when interpreting the results from experiments using the Ntsr1-Cre GN220 mouse for investigating corticothalamic neuronal function.

    sted, utgiver, år, opplag, sider
    ELSEVIER IRELAND LTD, 2018
    Emneord
    Corticothalamic; White matter; Neurotensin receptor 1; Layer 6; Visual cortex; Forkhead box protein 2
    HSV kategori
    Identifikatorer
    urn:nbn:se:liu:diva-148387 (URN)10.1016/j.neulet.2018.03.053 (DOI)000432759500007 ()29580883 (PubMedID)
    Merknad

    Funding Agencies|Swedish Research Council [3050, 2862]; Linkoping University

    Tilgjengelig fra: 2018-06-15 Laget: 2018-06-15 Sist oppdatert: 2018-10-12
    Fulltekst (pdf)
    Neuromodulation, Short-Term and Long-Term Plasticity in Corticothalamic and Hippocampal Neuronal Networks
    Download (pdf)
    omslag
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    presentationsbild
  • 290.
    Sundberg, Sofie
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelning för neurobiologi. Linköpings universitet, Medicinska fakulteten.
    Granseth, Björn
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelning för neurobiologi. Linköpings universitet, Medicinska fakulteten.
    Cre-expressing neurons in the cortical white matter of Ntsr1-Cre GN220 mice2018Inngår i: Neuroscience Letters, ISSN 0304-3940, E-ISSN 1872-7972, Vol. 675, s. 36-40Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Genetically modified mouse strains that express Cre-recombinase in specific neuronal sub-populations have become widely used tools for investigating neuronal function. The Ntsr1-Cre GN220 mouse expresses this enzyme in corticothalamic neurons in layer 6 of cerebral cortex. We observed that about 7% of Cre-expressing cells in the primary visual cortex are found within the white matter bordering layer 6. By using the immunohistochemical marker for layer 6 neurons, Forkhead box protein 2 (FoxP2), and fluorescently conjugated latex beads injected into the dorsal lateral geniculate nucleus, we show that about half of these cells are similar to and could belong to the layer 6 corticothalamic neuron population. The other half seems to be a distinct white matter (WM) neuron sub-population that we estimate to constitute 2-4% of the total cortical Cre expressing population. Staining for the neuronal marker Neuronal nuclei (NeuN) revealed that about 15-40% of WM neurons are Cre-expressing. Thus, the potential contribution from WM neurons needs to be considered when interpreting the results from experiments using the Ntsr1-Cre GN220 mouse for investigating corticothalamic neuronal function.

  • 291.
    Sundberg, Sofie
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelning för neurobiologi. Linköpings universitet, Medicinska fakulteten.
    Lindström, Sarah
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för Kirurgi, Ortopedi och Onkologi. Linköpings universitet, Medicinska fakulteten.
    Sanchez, Gonzalo Manuel
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelning för neurobiologi. Linköpings universitet, Medicinska fakulteten.
    Granseth, Björn
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelning för neurobiologi. Linköpings universitet, Medicinska fakulteten.
    Cre-expressing neurons in visual cortex of Ntsr1-Cre GN220 mice are corticothalamic and are depolarized by acetylcholine2018Inngår i: Journal of Comparative Neurology, ISSN 0021-9967, E-ISSN 1096-9861, Vol. 526, nr 1, s. 120-132Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The Ntsr1-Cre GN220 mouse expresses Cre-recombinase in corticothalamic (CT) neurons in neocortical layer 6. It is not known if the other major types of pyramidal neurons in this layer also express this enzyme. By electrophysiological recordings in slices and histological analysis of the uptake of retrogradely transported beads we show that Cre-positive neurons are CT and not corticocortical or corticoclaustral types. Furthermore, we show that Ntsr1-Cre-positive cells are immuno-positive for the nuclear transcription factor Forkhead box protein P2 (FoxP2). We conclude that Cre-expression is limited to a specific type of pyramidal neuron: CT. However, it appears as not all CT neurons are Cre-expressing; there are indications that the penetrance of the gene is about 90%. We demonstrate the utility of assigning a specific identity to individual neurons by determining that the CT neurons are potently modulated by acetylcholine acting on both nicotinic and muscarinic acetylcholine receptors. These results corroborate the suggested function of these neurons in regulating the gain of thalamocortical transfer of sensory information depending on attentional demand and state of arousal.

  • 292.
    Sörqvist, Patrik
    et al.
    Linköpings universitet, Institutionen för beteendevetenskap, Avdelningen för kognition, utveckling och handikapp, CDD. Linköpings universitet, Filosofiska fakulteten. University of Gavle, Sweden.
    Dahlström, Örjan
    Linköpings universitet, Institutionen för beteendevetenskap och lärande, Handikappvetenskap. Linköpings universitet, Filosofiska fakulteten. Linköpings universitet, Institutet för handikappvetenskap (IHV).
    Karlsson, Thomas
    Linköpings universitet, Institutionen för beteendevetenskap och lärande, Handikappvetenskap. Linköpings universitet, Filosofiska fakulteten.
    Rönnberg, Jerker
    Linköpings universitet, Institutionen för beteendevetenskap och lärande, Handikappvetenskap. Linköpings universitet, Filosofiska fakulteten. Linköpings universitet, Institutet för handikappvetenskap (IHV).
    Concentration: The Neural Underpinnings of How Cognitive Load Shields Against Distraction2016Inngår i: Frontiers in Human Neuroscience, ISSN 1662-5161, E-ISSN 1662-5161, Vol. 10, nr 221Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Whether cognitive load and other aspects of task difficulty increases or decreases distractibility is subject of much debate in contemporary psychology. One camp argues that cognitive load usurps executive resources, which otherwise could be used for attentional control, and therefore cognitive load increases distraction. The other camp argues that cognitive load demands high levels of concentration (focal task engagement), which suppresses peripheral processing and therefore decreases distraction. In this article, we employed an functional magnetic resonance imaging (fMRI) protocol to explore whether higher cognitive load in a visually-presented task suppresses task-irrelevant auditory processing in cortical and subcortical areas. The results show that selectively attending to an auditory stimulus facilitates its neural processing in the auditory cortex, and switching the locus-of-attention to the visual modality decreases the neural response in the auditory cortex. When the cognitive load of the task presented in the visual modality increases, the neural response to the auditory stimulus is further suppressed, along with increased activity in networks related to effortful attention. Taken together, the results suggest that higher cognitive load decreases peripheral processing of task-irrelevant information which decreases distractibility as a side effect of the increased activity in a focused-attention network.

    Fulltekst (pdf)
    fulltext
  • 293.
    Tarun, Anjali
    et al.
    Ecole Polytech Fed Lausanne, Switzerland; Univ Geneva, Switzerland.
    Behjat, Hamid
    Linköpings universitet, Centrum för medicinsk bildvetenskap och visualisering, CMIV.
    Bolton, Thomas
    Ecole Polytech Fed Lausanne, Switzerland; Univ Geneva, Switzerland.
    Abramian, David
    Linköpings universitet, Institutionen för medicinsk teknik, Avdelningen för medicinsk teknik. Linköpings universitet, Tekniska fakulteten. Lund Univ, Sweden.
    Van De Ville, Dimitri
    Ecole Polytech Fed Lausanne, Switzerland; Univ Geneva, Switzerland.
    Structural mediation of human brain activity revealed by white-matter interpolation of fMRI2020Inngår i: NeuroImage, ISSN 1053-8119, E-ISSN 1095-9572, Vol. 213, artikkel-id 116718Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Understanding how the anatomy of the human brain constrains and influences the formation of large-scale functional networks remains a fundamental question in neuroscience. Here, given measured brain activity in gray matter, we interpolate these functional signals into the white matter on a structurally-informed high-resolution voxel-level brain grid. The interpolated volumes reflect the underlying anatomical information, revealing white matter structures that mediate the interaction between temporally coherent gray matter regions. Functional connectivity analyses of the interpolated volumes reveal an enriched picture of the default mode network (DMN) and its subcomponents, including the different white matter bundles that are implicated in their formation, thus extending currently known spatial patterns that are limited within the gray matter only. These subcomponents have distinct structure-function patterns, each of which are differentially observed during tasks, demonstrating plausible structural mechanisms for functional switching between task-positive and -negative components. This work opens new avenues for the integration of brain structure and function, and demonstrates the collective mediation of white matter pathways across short and long-distance functional connections.

    Fulltekst (pdf)
    fulltext
  • 294.
    Taxén, Lars
    Linköpings universitet, Institutionen för datavetenskap. Linköpings universitet, Tekniska högskolan.
    The Activity Modalities: A Priori Categories of Coordination2015Inngår i: Proceedings of the Fourth International Conference on Cognitive Neurodynamics - 2013 / [ed] Hans Liljenström, Springer Publishing Company, 2015, Vol. 1, s. 21-29Konferansepaper (Fagfellevurdert)
    Abstract [en]

    A conceptualization of a-priori forms of coordination as activity modalities is proposed. Sensations in various sensory modalities are integrated by our brain into a coherent, actionable percept, structured by the processes of objectivation, contextualization, spatialization, temporalization, stabilization, and transition. This conceptualization promises to bridge neuroscientific and applied research into the coordination problem. 

    Fulltekst (pdf)
    fulltext
  • 295.
    Tegern, Gunilla
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Hälsa och samhälle. Linköpings universitet, Filosofiska fakulteten.
    Flodmark, O
    Department of Clinical Neuroscience, Karolinska Institute; Dept of Neuroradiology, Karolinska Hospital, Stockholm, Sweden.
    Psychological, social and economic consequences of incidental discovery of aneurysm2003Inngår i: Rivista di neuroradiologia, ISSN 1120-9976, Vol. 16, nr 5, s. 739-742Artikkel i tidsskrift (Fagfellevurdert)
  • 296. Bestill onlineKjøp publikasjonen >>
    Theodorsson, Annette
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Klinisk kemi. Linköpings universitet, Hälsouniversitetet.
    Estrogen-inducible neuropeptides in the rat brain: role in focal ischemic lesions2005Doktoravhandling, med artikler (Annet vitenskapelig)
    Abstract [en]

    Sex steroids in general and estrogens in particular – in addition to their effects on the reproductive organs – affect a large number of crucial bodily functions, including “higher” brain functions.

    Neuropeptides constitute the phylogenetically oldest neurotransmitter system and are currently thought to act mainly during stress, disease or injury. The concentration of galanin is i.a. up-regulated by injury to the nervous system and by estrogen.

    The main focus of the present thesis was to investigate whether the reported neuroprotective effect of 17β-estradiol in experimental animal stroke models is partially mediated through its effects on galanin and if galanin per se exerts neuroprotective effects in stroke.

    An exploratory study of the effects of sex steroid concentrations due to gender and pubertal development showed differences in concentrations of i.a. the neuropeptides galanin and neuropeptide Y also in brain regions of female rats important for higher brain functions, including hippocampus and cortex, brain regions not directly involved in reproduction. Puberty brings about changes in several hormonal mechanisms, and our studies showed that the major effect on the concentrations of galanin in various brain regions of ovariectomized (ovx) rats, was brought about by 17β-estradiol.

    The pathophysiological mechanisms involved in thrombolysis – the current treatment of choice in human stroke – attempts the re-establishment of perfusion (reperfusion) to the lesioned area of the brain. This prompted us to develop a reperfusion stroke model in rats designed to be mild, focal and transient, allowing long-term observation periods of animals thriving well postoperatively. Mortality and morbidity during and after the middle cerebral artery (MCA) occlusion are important confounding factors crucial for the results. Changing anaesthesia from intraperitoneally administered chloral hydrate to isofl urane inhalation anaesthesia using endotracheal intubation and controlled ventilation markedly reduced the mortality rate from 25% to 10.6%, which was even further reduced down to 2.7 % by successively improved surgical skills.

    Contrary to our initial hypothesis, long-term 17β-estradiol treatment resulted in larger ischemic lesions in our stroke model compared to control treatment. After 3 days the cerebral ischemic lesion area was doubled after 17β-estradiol treatment in rats subjected to 60 min microclip occlusion of the MCA followed by reperfusion. A similar, but not statistically signifi cant difference was found after 7 and 14 days. Three groups studying different types of experimental animal stroke and different doses of 17β-estradiol treatment have recently also demonstrated lack of neuroprotection by 17β-estradiol treatment. Furthermore, large epidemiological clinical studies have recently also reported an increased risk and poorer outcome in postmenopausal women subjected to hormone replacement therapy.

    The concentrations of galanin-like immunoreactivity in extracts of punch biopsies from the penumbra area after transient MCA occlusion were found unchanged, but were decreased (p=0.015) in the apparently undamaged ipsilateral hippocampus. Galanin administered by continuous intracerebroventricular infusion (2.4 nmol/day) resulted in a 30% larger ischemic lesion compared to controls, measured 7 days after the MCA occlusion. Taken together, these results indicate that galanin in the brain is primarily a factor reacting to ischemic injury rather than a neuroprotective factor in its own right.

    Very limited information is available about the steady state serum concentrations of 17β-estradiol in response to different modes of administration to rats for days and weeks. The need for this information has become especially apparent during recent years due to the observable dichotomy of estrogens effects – neuroprotective or not – in the various animal models of brain ischemia reported in the current scientific literature. The cause of this dichotomy is likely to be found in the experimental setup, including the mode of administration of 17β-estradiol. Delayed steady state of serum 17β-estradiol concentrations were found when comparing two common modes of exogenous administration of 17β-estradiol – slow-release osmotic pumps vs. daily subcutaneously injections of 17β-estradiol solved in sesame oil – to ovx rats during 2 times 6 weeks crossover treatment. Steady state was reached at week 4 in the daily injections group compared to at week 6 in the slow release osmotic pumps group. Once steady state was reached, the concentration was the same in both groups for the reminder of the experiment (in total 12 weeks).

    Delarbeid
    1. Sex differences in neuropeptide distribution in the rat brain
    Åpne denne publikasjonen i ny fane eller vindu >>Sex differences in neuropeptide distribution in the rat brain
    Vise andre…
    1999 (engelsk)Inngår i: Peptides, ISSN 0196-9781, E-ISSN 1873-5169, Vol. 20, nr 1, s. 81-86Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    We have investigated possible sex differences in the regional concentrations of neuropeptides in the rat brain. Immunoreactive neurotensin (NT), neurokinin A (NKA), galanin (GAL), calcitonin gene-related peptide (CGRP), substance P (SP) and neuropeptide Y (NPY) were measured by radioimmunoassay in frontal cortex, occipital cortex, hippocampus, striatum, hypothalamus and pituitary in male and female pre- and postpubertal rats. Sex differences were found for NPY (p < 0.001), NT (p < 0.01) and GAL (p < 0.05), in particular in hippocampus, striatum, hypothalamus and pituitary, but not for CGRP, SP and NKA. Results from analysis of neuropeptides in one sex may not be entirely applicable to the other.

    Emneord
    Sex differences, Neuropeptide Y, Neurotensin, Galanin, Hippocampus, Pituitary, Frontal cortex, Puberty
    HSV kategori
    Identifikatorer
    urn:nbn:se:liu:diva-13441 (URN)10.1016/S0196-9781(98)00139-9 (DOI)
    Tilgjengelig fra: 2005-11-11 Laget: 2005-11-11 Sist oppdatert: 2017-12-13bibliografisk kontrollert
    2. Effects of estradiol, progesterone, and norethisterone on regional concentrations of galanin in the rat brain
    Åpne denne publikasjonen i ny fane eller vindu >>Effects of estradiol, progesterone, and norethisterone on regional concentrations of galanin in the rat brain
    1999 (engelsk)Inngår i: Peptides, ISSN 0196-9781, E-ISSN 1873-5169, Vol. 20, nr 6, s. 743-748Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    Concentrations of immunoreactive galanin were compared in eight gross brain regions of ovariectomized female rats treated with either estradiol, estradiol + progesterone, estradiol + norethisterone, or placebo. Higher concentrations with estradiol treatment compared with placebo were found in the pituitary (357%), frontal cortex (162%), occipital cortex (174%), hippocampus (170%), and median eminence (202%). A more profound difference with addition of progesterone or norethisterone was seen in the pituitary (529% and 467%, respectively). Sex steroids, particularly estradiol, modulate galanin concentrations not only in reproductive, but also in nonreproductive, brain regions.

    Emneord
    Galanin, Estradiol, Progesterone, Norethisterone, Hippocampus, Pituitary, Frontal cortex
    HSV kategori
    Identifikatorer
    urn:nbn:se:liu:diva-13442 (URN)10.1016/S0196-9781(99)00057-1 (DOI)
    Tilgjengelig fra: 2005-11-11 Laget: 2005-11-11 Sist oppdatert: 2017-12-13bibliografisk kontrollert
    3. Modern anesthesia and peroperative monitoring methods reduce per- and postoperative mortality during transient occlusion of the middle cerebral artery in rats
    Åpne denne publikasjonen i ny fane eller vindu >>Modern anesthesia and peroperative monitoring methods reduce per- and postoperative mortality during transient occlusion of the middle cerebral artery in rats
    2005 (engelsk)Inngår i: Brain Research Protocols, ISSN 1385-299X, E-ISSN 1872-809X, Vol. 14, nr 3, s. 181-190Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    Mortality and morbidity during and after occlusion of the middle cerebral artery in rats are important confounding factors which may be minimized by improved anesthesia and peroperative monitoring techniques. We describe state of the art techniques for inducing anesthesia, endotracheal intubation, ventilation and monitoring peroperatively in this context.

    Introducing the subtemporal approach of Tamura et al. in our laboratory 5 years ago, we experienced 25% peroperative and 24 h postoperative rat mortality when performing temporary clipping of the middle cerebral artery. This prompted us to abandon intraperitoneal anesthesia by chloral hydrate and ventilation by tracheotomy in favor of endotracheal intubation and isoflurane anesthesia (1% isoflurane in 30%:70% O2/N2O). These anesthetic techniques in combination with improved surgical skills have reduced our initial 25% peroperative- and 24 h postoperative mortality to 2.7% (1.8% peroperatively and 0.9% 24 h postoperatively). Furthermore, the following 14 days postoperative mortality rate was 1.8%. A total number of 203 rats have been operated with this method in different studies where a focal reperfusion stroke model combined with extended periods of observations were the cornerstone.

    Emneord
    Cerebral ischemia; Focal; Middle cerebral artery occlusion; Anesthetic method; Isoflurane; Rat
    HSV kategori
    Identifikatorer
    urn:nbn:se:liu:diva-13443 (URN)10.1016/j.brainresprot.2005.01.002 (DOI)
    Tilgjengelig fra: 2005-11-11 Laget: 2005-11-11 Sist oppdatert: 2017-12-13bibliografisk kontrollert
    4. Serum concentrations of 17β-estradiol in ovariectomized rats during 2 times 6 weeks crossover treatment by daily injections in comparison with slow-release pellets
    Åpne denne publikasjonen i ny fane eller vindu >>Serum concentrations of 17β-estradiol in ovariectomized rats during 2 times 6 weeks crossover treatment by daily injections in comparison with slow-release pellets
    Vise andre…
    2005 (engelsk)Inngår i: Scandinavian Journal of Clinical and Laboratory Investigation, ISSN 1502-7686 (electronic) 0036-5513 (paper), Vol. 65, nr 8, s. 699-706Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    Estrogens exert widespread biological functions that reach far beyond their well-known role in reproduction. Exogenous administration of 17β-estradiol to ovariectomized experimental animals is of the utmost importance in elucidating its mechanisms of action. In the present study, we compared two different modes of exogenous administration of 17β-estradiol to ovariectomized rats in relation to the serum 17β-estradiol concentrations over prolonged periods of time. 17β-estradiol was administered either by slow-release pellets (Innovative Research of America, Sarasota, Fl. 34236, USA, 90-day release, NHH-115, 1.5 mg) or by daily subcutaneous injections of 15 µg 17β-estradiol dissolved in sesame oil. After 6 weeks, the mode of administration of estradiol was changed to the opposite method and continued for a further 6 weeks. Blood samples for measurement of serum 17β-estradiol were taken every second week. After 2 weeks, the serum concentrations of 17β-estradiol in group A initially receiving the pellets were 73 % higher (p<0.001) compared to those of group B receiving daily injections. The difference was even more prominent, 580 % (p<0.001), after 4 weeks. Steady state was reached at week 6 in group A, but already by week 4 in group B. Once steady state was reached, the concentrations were the same in both groups for the remainder of the experiment (12 weeks in total). Our study indicates that steady-state concentrations of 17β-estradiol occur 5-6 weeks later than the 48 h the manufacturer of the slow-release pellets claims.

    Emneord
    Estrogen; 17β-estradiol; rat; slow-release pellet
    HSV kategori
    Identifikatorer
    urn:nbn:se:liu:diva-13444 (URN)10.1080/00365510500375206 (DOI)
    Tilgjengelig fra: 2005-11-11 Laget: 2005-11-11 Sist oppdatert: 2018-01-26
    5. Estradiol increases brain lesions in the cortex and lateral striatum after transient occlusion of the middle cerebral artery in rats: No effect of ischemia on galanin in the stroke area but decreased levels in the hippocampus
    Åpne denne publikasjonen i ny fane eller vindu >>Estradiol increases brain lesions in the cortex and lateral striatum after transient occlusion of the middle cerebral artery in rats: No effect of ischemia on galanin in the stroke area but decreased levels in the hippocampus
    2005 (engelsk)Inngår i: Peptides, ISSN 0196-9781, Vol. 26, nr 11, s. 2257-2264Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    A distinctive feature of galanin expression is that it is extensively increased by neuronal injury, estrogens, Alzheimer's disease and during development. Since stroke is amongst the clinically most important causes of neuronal injury we studied the tissue concentrations of galanin in a rat stroke model and the possibility of modulating this effect with estrogen. Transient focal middle cerebral artery ischemia was induced in rats that 2 weeks earlier underwent ovariectomy and received 1.5 mg 17β-estradiol slow-release or placebo pellets. The concentrations of galanin and neuropeptide Y were measured after observation periods of 3, 7 and 14 days in extracts of punch biopsies from both the lesioned and the contra lateral control hemisphere. The galanin levels were not changed in any of the brain regions studied except in the hippocampus where they were lower in the ischemic hemisphere in both the estrogen- and placebo-treated animals compared to the corresponding contra lateral intact hemisphere (p = 0.015). Estrogen treatment up-regulated galanin concentrations in both the ventral and dorsal hippocampus (p = 0.003). The effects on the galanin concentrations were similar after all observation periods: 3, 7 and 14 days (p = 0.144). No significant changes were observed in the concentration of neuropeptide Y in response to the lesions. The ischemic lesions were markedly larger in the estrogen-treated animals observed after 3 days compared to the corresponding control group. In the estrogen group the lesion was largest at bregma and the slice 2 mm anterior to the bregma, 82% and 435% larger than in the control group (p < 0.001). A similar, but much less pronounced (not statistically significant) difference was seen in the groups observed after 7 and 14 days. Earlier studies of lesions in the peripheral and central nervous systems have generally shown an up-regulation of galanin markers in response to but at a distance from the injury. Our results indicate that galanin is not involved in the response of the ischemic penumbra itself to stroke, whereas it may participate in the reactions of the neural stem-cell rich hippocampus to stroke.

    Emneord
    Galanin; Neuropeptide Y; Neuropeptides; Stroke; Cerebral ischemia; Estrogen; Neuroprotection; Middle cerebral artery occlusion; Rat
    HSV kategori
    Identifikatorer
    urn:nbn:se:liu:diva-13445 (URN)10.1016/j.peptides.2005.04.013 (DOI)
    Tilgjengelig fra: 2005-11-11 Laget: 2005-11-11 Sist oppdatert: 2009-06-05
    6. Galanin administered intracerebroventricularly increases ischemic lesions measured 7 days after focal and transient occlusion of the middle cerebral artery in female rats
    Åpne denne publikasjonen i ny fane eller vindu >>Galanin administered intracerebroventricularly increases ischemic lesions measured 7 days after focal and transient occlusion of the middle cerebral artery in female rats
    2005 (engelsk)Artikkel i tidsskrift (Fagfellevurdert) Submitted
    HSV kategori
    Identifikatorer
    urn:nbn:se:liu:diva-13446 (URN)
    Tilgjengelig fra: 2005-11-11 Laget: 2005-11-11
    Fulltekst (pdf)
    FULLTEXT01
  • 297.
    Thor, Stefan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Utvecklingsbiologi. Linköpings universitet, Hälsouniversitetet.
    Neuroscience: Light moulds plastic brains2008Inngår i: Nature, ISSN 0028-0836, E-ISSN 1476-4687, Vol. 456, nr 7219, s. 177-178Artikkel i tidsskrift (Annet vitenskapelig)
    Abstract [en]

    In tadpoles, the number of neurons expressing the neurotransmitter dopamine increases on exposure to light. Such plasticity might allow animals to physically match their brains’ activity to environmental stimuli.

    Fulltekst (pdf)
    FULLTEXT01
  • 298.
    Thor, Stefan
    et al.
    Molecular Neurobiology Laboratory, The Salk Institute, PO Box 85800, San Diego, California 92186, USA.
    Andersson, Siv G E
    Center for Neurobiology and Behavior, Department of Genetics and Development, College of Physicians and Surgeons of Columbia University, 701 West 168th Street, New York, New York 10032, USA.
    Tomlinson, Andrew
    Center for Neurobiology and Behavior, Department of Genetics and Development, College of Physicians and Surgeons of Columbia University, 701 West 168th Street, New York, New York 10032, USA.
    Thomas, John B
    Molecular Neurobiology Laboratory, The Salk Institute, PO Box 85800, San Diego, California 92186, USA.
    A LIM-homeodomain combinatorial code for motor-neuron pathway selection.1999Inngår i: Nature, ISSN 0028-0836, E-ISSN 1476-4687, Vol. 397, nr 6714, s. 76-80Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Different classes of vertebrate motor neuron that innervate distinct muscle targets express unique combinations of LIM-homeodomain transcription factors, suggesting that a combinatorial code of LIM-homeodomain proteins may underlie the control of motor-neuron pathway selection. Studies of LIM-homeodomain genes in mouse, Drosophila melanogaster and Caenorhabditis elegans have revealed functions of these genes in neuronal survival, axon guidance, neurotransmitter expression and neuronal function, but, to our knowledge, none of these studies have addressed the issue of a functional code. Here we study two members of this gene family in Drosophila, namely lim3, the homologue of the vertebrate Lhx3 and Lhx4 genes, and islet, the homologue of the vertebrate Isl1 and Is12 genes. We show that Drosophila lim3 is expressed by a specific subset of islet-expressing motor neurons and that mutating or misexpressing lim3 switches motor-neuron projections predictably. Our results provide evidence that lim3 and islet constitute a combinatorial code that generates distinct motor-neuron identities.

  • 299.
    Thorsell, Annika
    National Institute on Alcohol Abuse and Alcoholism, NIH; Bethesda, MD, USA.
    Brain neuropeptide Y and corticotropin-releasing hormone in mediating stress and anxiety2010Inngår i: Experimental biology and medicine (Maywood, N.J.: Print), ISSN 1535-3702, E-ISSN 1535-3699, Vol. 235, nr 10, s. 1163-1167Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Neuropeptides such as neuropeptide Y (NPY) and corticotropin-releasing hormone (CRH) have been implicated not only in acute regulation of stress/anxiety-related behaviors, but adaptations and changes in these neuropeptide systems may also participate in the regulation of behavior and endocrine responses during chronic stress. NPY is an endogenous anxiolytic neuropeptide, while CRH has anxiogenic properties upon central administration. Changes in these neuropeptide systems may contribute to disease states and give us indications for putative treatment targets for stress/anxiety disorders as well as alcohol/drug dependence. In this review, we briefly present these two systems and review their involvement in mediating the responses to acute and chronic stressors, as well as their possible roles in the development and progression of stress/anxiety disorders. We suggest that neuropeptides may be attractive in treatment development for stress/anxiety disorders, as well as for alcohol/drug dependence, based on their specificity and activity following exposure to external challenges, i.e. stressors, and their differential adaptations during transition from an acute to a chronic stress exposure state.

  • 300.
    Thorsell, Annika
    National Institute on Alcohol Abuse and Alcoholism, NIH; Bethesda, MD, USA.
    Central neuropeptide Y in anxiety- and stress-related behavior and in ethanol intake2008Inngår i: Annals of the New York Academy of Sciences, ISSN 0077-8923, E-ISSN 1749-6632, Vol. 1148, s. 136-140Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    One of the most profound properties of central neuropeptide Y (NPY) is its anxiolytic, or anti-anxiety, effect. This has been demonstrated repeatedly in a number of animal models. In addition, stressors affect NPY expression in the central nervous system, with acute and repeated (chronic) stress having differential effects. Here, a brief summary of some work performed in our laboratory is presented that supports a role for NPY in regulation of stress responses and behaviors.

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