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Shionoya, Kiseko
Publications (10 of 24) Show all publications
Zajdel, J., Zager, A., Blomqvist, A., Engblom, D. & Shionoya, K. (2019). Acute maternal separation potentiates the gene expression and corticosterone response induced by inflammation. Brain, behavior, and immunity, 77, 141-149
Open this publication in new window or tab >>Acute maternal separation potentiates the gene expression and corticosterone response induced by inflammation
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2019 (English)In: Brain, behavior, and immunity, ISSN 0889-1591, E-ISSN 1090-2139, Vol. 77, p. 141-149Article in journal (Refereed) Published
Abstract [en]

Maternal care is crucial for infants and profoundly affects their responses to different kinds of stressors. Here, we examined how maternal separation affects inflammatory gene expression and the corticosterone response to an acute immune challenge induced by lipopolysaccharide (LPS; 40 µg/kg ip) in mouse pups, 8–9 days old. Maternal separation initially attenuated LPS-induced hypothalamic pro-inflammatory gene expression, but later, at 3 h after immune challenge, robustly augmented such gene expression and increased serum corticosterone levels. Providing the pups with a warm and soft object prevented the separation-induced augmented hypothalamic-pituitary-adrenal (HPA)-axis response. It also prevented the potentiated induction of some, but not all, inflammatory genes to a similar extent as did the dam. Our results show that maternal separation potentiates the inflammatory response and the resulting HPA-axis activation, which may have detrimental effects if separation is prolonged or repeated.

Place, publisher, year, edition, pages
Elsevier, 2019
Keywords
Lipopolysaccharide, Hypothalamus, Cytokines, Inflammation, Maternal separation, Corticosterone
National Category
Pharmacology and Toxicology Developmental Biology Medical Biotechnology Immunology
Identifiers
urn:nbn:se:liu:diva-154886 (URN)10.1016/j.bbi.2018.12.016 (DOI)30590109 (PubMedID)2-s2.0-85059128986 (Scopus ID)
Available from: 2019-03-04 Created: 2019-03-04 Last updated: 2019-04-08Bibliographically approved
Klawonn, A., Fritz, M., Nilsson, A., Bonaventura, J., Shionoya, K., Mirrasekhian, E., . . . Engblom, D. (2018). Motivational valence is determined by striatal melanocortin 4 receptors. Journal of Clinical Investigation, 128(7), 3160-3170
Open this publication in new window or tab >>Motivational valence is determined by striatal melanocortin 4 receptors
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2018 (English)In: Journal of Clinical Investigation, ISSN 0021-9738, E-ISSN 1558-8238, Vol. 128, no 7, p. 3160-3170Article in journal (Refereed) Published
Abstract [en]

It is critical for survival to assign positive or negative valence to salient stimuli in a correct manner. Accordingly, harmful stimuli and internal states characterized by perturbed homeostasis are accompanied by discomfort, unease, and aversion. Aversive signaling causes extensive suffering during chronic diseases, including inflammatory conditions, cancer, and depression. Here, we investigated the role of melanocortin 4 receptors (MC4Rs) in aversive processing using genetically modified mice and a behavioral test in which mice avoid an environment that they have learned to associate with aversive stimuli. In normal mice, robust aversions were induced by systemic inflammation, nausea, pain, and. opioid receptorinduced dysphoria. In sharp contrast, mice lacking MC4Rs displayed preference or indifference toward the aversive stimuli. The unusual flip from aversion to reward in mice lacking MC4Rs was dopamine dependent and associated with a change from decreased to increased activity of the dopamine system. The responses to aversive stimuli were normalized when MC4Rs were reexpressed on dopamine D1 receptor-expressing cells or in the striatum of mice otherwise lacking MC4Rs. Furthermore, activation of arcuate nucleus proopiomelanocortin neurons projecting to the ventral striatum increased the activity of striatal neurons in an MC4R-dependent manner and elicited aversion. Our findings demonstrate that melanocortin signaling through striatal MC4Rs is critical for assigning negative motivational valence to harmful stimuli.

Place, publisher, year, edition, pages
AMER SOC CLINICAL INVESTIGATION INC, 2018
National Category
Neurosciences
Identifiers
urn:nbn:se:liu:diva-149861 (URN)10.1172/JCI97854 (DOI)000437234600044 ()29911992 (PubMedID)
Note

Funding Agencies|European Research Council; Swedish Medical Research Council; Knut and Alice Wallenberg Foundation; Swedish Brain foundation; County Council of Ostergotland; National Institute on Drug Abuse Intramural Research Program [ZIA000069]; Lars Hiertas Minne Foundation

Available from: 2018-08-02 Created: 2018-08-02 Last updated: 2018-08-20
Mirrasekhian, E., Nilsson, J. L. Å., Shionoya, K., Blomgren, A., Zygmunt, P. M., Engblom, D., . . . Blomqvist, A. (2018). The antipyretic effect of paracetamol occurs independent of transient receptor potential ankyrin 1–mediated hypothermia and is associated with prostaglandin inhibition in the brain. The FASEB Journal
Open this publication in new window or tab >>The antipyretic effect of paracetamol occurs independent of transient receptor potential ankyrin 1–mediated hypothermia and is associated with prostaglandin inhibition in the brain
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2018 (English)In: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860Article in journal (Refereed) Published
Abstract [en]

The mode of action of paracetamol (acetaminophen), which is widely used for treating pain and fever, has remained obscure, but may involve several distinct mechanisms, including cyclooxygenase inhibition and transient receptor potential ankyrin 1 (TRPA1) channel activation, the latter being recently associated with paracetamol?s propensity to elicit hypothermia at higher doses. Here, we examined whether the antipyretic effect of paracetamol was due to TRPA1 activation or cyclooxygenase inhibition. Treatment of wild-type and TRPA1 knockout mice rendered febrile by immune challenge with LPS with a dose of paracetamol that did not produce hypothermia (150 mg/kg) but is known to be analgetic, abolished fever in both genotypes. Paracetamol completely suppressed the LPS-induced elevation of prostaglandin E2 in the brain and also reduced the levels of several other prostanoids. The hypothermia induced by paracetamol was abolished in mice treated with the electrophile-scavenger N-acetyl cysteine. We conclude that paracetamol?s antipyretic effect in mice is dependent on inhibition of cyclooxygenase activity, including the formation of pyrogenic prostaglandin E2, whereas paracetamol-induced hypothermia likely is mediated by the activation of TRPA1 by electrophilic metabolites of paracetamol, similar to its analgesic effect in some experimental paradigms.?Mirrasekhian, E., Nilsson, J. L. Å., Shionoya, K., Blomgren, A., Zygmunt, P. M., Engblom, D., Högestätt, E. D., Blomqvist, A. The antipyretic effect of paracetamol occurs independent of transient receptor potential ankyrin 1?mediated hypothermia and is associated with prostaglandin inhibition in the brain.

Place, publisher, year, edition, pages
Federation of American Societies for Experimental Biology, 2018
National Category
Pharmacology and Toxicology
Identifiers
urn:nbn:se:liu:diva-148562 (URN)10.1096/fj.201800272R (DOI)000447972500045 ()29738273 (PubMedID)
Note

Funding agencies: Swedish Medical Research Council [20725, 07879, 2014-3801]; European Research Council (ERC) Starting Grant; Knut and Alice Wallenberg Foundation; Swedish Brain Foundation; Swedish Cancer Foundation [16/0572]; County Council of Ostergotland; Medical Facult

Available from: 2018-06-13 Created: 2018-06-13 Last updated: 2018-11-09Bibliographically approved
Matsuwaki, T., Shionoya, K., Ihnatko, R., Eskilsson, A., Kakuta, S., Dufour, S., . . . Blomqvist, A. (2017). Involvement of interleukin-1 type 1 receptors in lipopolysaccharide-induced sickness responses. Brain, behavior, and immunity, 66, 165-176
Open this publication in new window or tab >>Involvement of interleukin-1 type 1 receptors in lipopolysaccharide-induced sickness responses
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2017 (English)In: Brain, behavior, and immunity, ISSN 0889-1591, E-ISSN 1090-2139, Vol. 66, p. 165-176Article in journal (Refereed) Published
Abstract [en]

Sickness responses to lipopolysaccharide (LPS) were examined in mice with deletion of the interleukin (IL)-1 type 1 receptor (IL-1R1). IL-1R1 knockout (1(0) mice displayed intact anorexia and HPA-axis activation to intraperitoneally injected LPS (anorexia: 10 or 120 mu g/kg; HPA-axis: 120 mu g/kg), but showed attenuated but not extinguished fever (120 g/kg). Brain PGE2 synthesis was attenuated, but Cox-2 induction remained intact. Neither the tumor necrosis factor-alpha (TNF alpha) inhibitor etanercept nor the IL -6 receptor antibody tocilizumab abolished the LPS induced fever in IL -1R1 KO mice. Deletion of IL -1R1 specifically in brain endothelial cells attenuated the LPS induced fever, but only during the late, 3rd phase of fever, whereas deletion of IL-1R1 on neural cells or on peripheral nerves had little or no effect on the febrile response. We conclude that while IL-1 signaling is not critical for LPS induced anorexia or stress hormone release, IL-1R1, expressed on brain endothelial cells, contributes to the febrile response to LPS. However, also in the absence of IL-1R1, LPS evokes a febrile response, although this is attenuated. This remaining fever seems not to be mediated by IL-6 receptors or TNFa, but by some yet unidentified pyrogenic factor. 

Place, publisher, year, edition, pages
Elsevier, 2017
Keywords
Interleukin-1 type 1 receptor; Lipopolysaccharide; Fever; Anorexia; ACTH; Corticosterone; Endothelial cells; THF alpha; Interleukin-6; PGE(2)
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:liu:diva-143084 (URN)10.1016/j.bbi.2017.06.013 (DOI)000414236600018 ()28655587 (PubMedID)
Note

Funding Agencies|Japan Society for the Promotion of Science [15K18800]; Swedish Research Council [20725, 07879]; Knut and Alice Wallenberg foundation; Swedish Brain Foundation; Swedish Cancer Foundation [213/692]; County Council of Ostergotland; Sixth Research Framework Programme of the European Union, Project MUGEN [MUGEN LSHG-CT-2005-005203]; MRC research grant [G0801296]

Available from: 2017-11-22 Created: 2017-11-22 Last updated: 2018-06-18
Ericsson, M., Henriksen, R., Bélteky, J., Sundman, A.-S., Shionoya, K. & Jensen, P. (2016). Long-Term and Transgenerational Effects of Stress Experienced during Different Life Phases in Chickens (Gallus gallus). PLoS ONE, 11(4), Article ID e0153879.
Open this publication in new window or tab >>Long-Term and Transgenerational Effects of Stress Experienced during Different Life Phases in Chickens (Gallus gallus)
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2016 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 11, no 4, article id e0153879Article in journal (Refereed) Published
Abstract [en]

Stress in animals causes not only immediate reactions, but may affect their biology for long periods, even across generations. Particular interest has been paid to perinatal stress, but also adolescence has been shown to be a sensitive period in mammals. So far, no systematic study has been performed of the relative importance of stress encountered during different life phases. In this study, groups of chickens were exposed to a six-day period of repeated stress during three different life phases: early (two weeks), early puberty (eight weeks) and late puberty (17 weeks), and the effects were compared to an unstressed control group. The short-term effects were assessed by behaviour, and the long-term and transgenerational effects were determined by effects on behavior and corticosterone secretion, as well as on hypothalamic gene expression. Short-term effects were strongest in the two week group and the eight week group, whereas long-term and transgenerational effects were detected in all three stress groups. However, stress at different ages affected different aspects of the biology of the chickens, and it was not possible to determine a particularly sensitive life phase. The results show that stress during puberty appears to be at least equally critical as the previously studied early life phase. These findings may have important implications for animal welfare in egg production, since laying hens are often exposed to stress during the three periods pinpointed here.

Place, publisher, year, edition, pages
Plos One, 2016
National Category
Developmental Biology Cell Biology
Identifiers
urn:nbn:se:liu:diva-127492 (URN)10.1371/journal.pone.0153879 (DOI)000374565100026 ()27105229 (PubMedID)
Funder
Swedish Research Council, 621-2011-4731 (PJ)Swedish Research Council Formas, 221-2011-1088 (PJ)EU, European Research Council, 322206 (PJ)
Note

Funding agencies: Swedish Research Council [621-2011-4731]; Swedish Research Council for Environment, Agricultural Sciences and Spatial Planning [221-2011-1088]; European Research Council [322206]

Available from: 2016-04-28 Created: 2016-04-28 Last updated: 2017-11-30Bibliographically approved
Rincon-Cortes, M., Barr, G. A., Marie Mouly, A., Shionoya, K., Nunez, B. S. & Sullivan, R. M. (2015). Enduring good memories of infant trauma: Rescue of adult neurobehavioral deficits via amygdala serotonin and corticosterone interaction. Proceedings of the National Academy of Sciences of the United States of America, 112(3), 881-886
Open this publication in new window or tab >>Enduring good memories of infant trauma: Rescue of adult neurobehavioral deficits via amygdala serotonin and corticosterone interaction
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2015 (English)In: Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, E-ISSN 1091-6490, Vol. 112, no 3, p. 881-886Article in journal (Refereed) Published
Abstract [en]

Children form a strong attachment to their caregiver-even when that caretaker is abusive. Paradoxically, despite the trauma experienced within this relationship, the child develops a preference for trauma-linked cues-a phenomenon known as trauma bonding. Although infant trauma compromises neurobehavioral development, the mechanisms underlying the interaction between infant trauma bonding (i.e., learned preference for trauma cues) and the long-term effects of trauma (i.e., depressive-like behavior, amygdala dysfunction) are unknown. We modeled infant trauma bonding by using odor-shock conditioning in rat pups, which engages the attachment system and produces a life-long preference for the odor that was paired with shock. In adulthood, this trauma-linked odor rescues depressive-like behavior and amygdala dysfunction, reduces corticosterone (CORT) levels, and exerts repair-related changes at the molecular level. Amygdala microarray after rescue implicates serotonin (5-HT) and glucocorticoids (GCs), and a causal role was verified through microinfusions. Blocking amygdala 5-HT eliminates the rescue effect; increasing amygdala 5-HT and blocking systemic CORT mimics it. Our findings suggest that infant trauma cues share properties with antidepressants and safety signals and provide insight into mechanisms by which infant trauma memories remain powerful throughout life.

Place, publisher, year, edition, pages
National Academy of Sciences, 2015
Keywords
infant trauma; amygdala; serotonin; depression; safety signal
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-114582 (URN)10.1073/pnas.1416065112 (DOI)000348040700063 ()25561533 (PubMedID)
Note

Funding Agencies|National Science Foundation [DGE-1137475]; [NIH-MH091451]; [NIH-DC009910]; [NIH-MH80603]

Available from: 2015-02-27 Created: 2015-02-26 Last updated: 2017-12-04
Sullivan, R. M., Moriceau, S., Roth, T. & Shionoya, K. (2014). Developmental Neurobiology of Olfactory Preference and Avoidance Learning. In: Mark S. Blumberg, John H. Freeman, and Scott R. Robinson (Ed.), Oxford Handbook of Developmental Behavioral Neuroscience: (pp. 573-587). Oxford: Oxford University Press
Open this publication in new window or tab >>Developmental Neurobiology of Olfactory Preference and Avoidance Learning
2014 (English)In: Oxford Handbook of Developmental Behavioral Neuroscience / [ed] Mark S. Blumberg, John H. Freeman, and Scott R. Robinson, Oxford: Oxford University Press, 2014, p. 573-587Chapter in book (Other academic)
Abstract [en]

Infants from a myriad of species attach to their caregiver regardless of the quality of care received, although the quality of care influences development of the stress system. To better understand this relationship, this chapter characterizes attachment learning and the supporting neural circuit in infant rat pups. During early life, odors paired with pain paradoxically produce subsequent approach responses to the odor and attachment. The neural circuit supporting this attachment learning involves the olfactory bulb encoding the preference learning and suppression of the amygdala to prevent the aversion learning. Increasing the stress hormone corticosterone during acquisition or decreasing endogenous opioids during consolidation prevents this odor approach learning. These data suggest that early life attachment is readily learned and supported by both increased opioids and decreased stress.

Place, publisher, year, edition, pages
Oxford: Oxford University Press, 2014
Series
Oxford Handbook of Developmental Behavioral Neuroscience ; 27
Keywords
Stress system, attachment learning, odors, pain, olfactory bulb, amygdale, corticosterone, endogenous opioids
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-150383 (URN)10.1093/oxfordhb/9780195314731.013.0028 (DOI)9780195314731 (ISBN)
Available from: 2018-08-21 Created: 2018-08-21 Last updated: 2018-09-03Bibliographically approved
Shionoya, K., Hegoburu, C., Brown, B., Sullivan, R., Doyère, V. & Mouly, A.-M. (2013). It’s time to fear! Interval timing in odor fear conditioning in rats. Frontiers in Behavioral Neuroscience, 7, Article ID 128.
Open this publication in new window or tab >>It’s time to fear! Interval timing in odor fear conditioning in rats
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2013 (English)In: Frontiers in Behavioral Neuroscience, ISSN 1662-5153, E-ISSN 1662-5153, Vol. 7, article id 128Article in journal (Refereed) Published
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.

Place, publisher, year, edition, pages
Frontiers Media S.A., 2013
Keywords
Odor fear conditioning, intervaltiming, amygdala, dopamine, respiration, ultrasonic vocalization, freezing
National Category
Neurosciences
Identifiers
urn:nbn:se:liu:diva-150378 (URN)10.3389/fnbeh.2013.00128 (DOI)000324909500001 ()24098277 (PubMedID)2-s2.0-84887560373 (Scopus ID)
Available from: 2018-08-21 Created: 2018-08-21 Last updated: 2018-08-28Bibliographically approved
Sullivan, R. M., Shionoya, K., Boulanger Bertolus, J., Ahers, J., Londen, E., Hegoburu, C., . . . Mouly, A.-M. (2012). Ontogenesis Of Time Interval Encoding In Odor Fear Conditioning. Paper presented at Abstracts: International Society for Developmental Psychobiology. Developmental Psychobiology, 54(7), 768-768
Open this publication in new window or tab >>Ontogenesis Of Time Interval Encoding In Odor Fear Conditioning
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2012 (English)In: Developmental Psychobiology, ISSN 0012-1630, E-ISSN 1098-2302, Vol. 54, no 7, p. 768-768Article in journal (Refereed) Published
Abstract [en]

In Pavlovian fear conditioning, an initially neutral stimulus predicts the arrival of an aversive stimulus at a fixed time interval. Accumulating evidence indicates that in associative learning temporal relations between events are encoded. However the neural networks underlying the encoding and memory of interval durations are poorly understood. We addressed this question in odor fear conditioning which can be performed in young pups as well as in adult animals. In this task, an odor is presented to the animal and after a fixed interval (30 seconds) a mild footshock is applied. We first investigated the ontogenesis of interval timing at the behavioral level. We designed an experimental setup allowing the simultaneous recording of respiration, ultrasonic vocalizations (USVs) and freezing in rats. These parameters greatly improved the sensitivity of fear behavior assessment, thus increasing the probability of detecting transient anticipatory fear responses. Three ages were considered: 14-days-old (infants), 22-days-old (juveniles) and 75-days-old (adults). The data show that in adults, an anticipator y response develops after a few odor-shock pairings, characterized by a decrease in respiratory rhythm and an increase in USVs emission prior to shock delivery. Similar anticipatory responses might be present in juveniles, while infants might show no signs of interval timing, despite showing good learning of the odor-shock association. In parallel, current experiments are investigating learning-induced brain activation at these three ages, using 2 Deoxyglucose metabolic mapping. We are focusing on structures known to be involved in timing in adults: striatum, nucleus accumbens and prefrontal cortex.

Place, publisher, year, edition, pages
John Wiley & Sons, 2012
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-150410 (URN)10.1002/dev.21076 (DOI)
Conference
Abstracts: International Society for Developmental Psychobiology
Available from: 2018-08-22 Created: 2018-08-22 Last updated: 2018-08-22Bibliographically approved
Gómez-Climent, M. Á., Hernández-González, S., Shionoya, K., Belles, M., Alonso-Llosa, G., Datiche, F. & Nacher, J. (2011). Olfactory bulbectomy, but not odor conditioned aversion, induces the differentiation of immature neurons in the adult rat piriform cortex. Neuroscience, 181(5), 18-27
Open this publication in new window or tab >>Olfactory bulbectomy, but not odor conditioned aversion, induces the differentiation of immature neurons in the adult rat piriform cortex
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2011 (English)In: Neuroscience, ISSN 0306-4522, E-ISSN 1873-7544, Vol. 181, no 5, p. 18-27Article in journal (Refereed) Published
Abstract [en]

The piriform cortex layer II of young-adult rats presents a population of prenatally generated cells, which express immature neuronal markers, such as the polysialylated form of the neural cell adhesion molecule (PSA-NCAM) or doublecortin (DCX), and display structural characteristics of immature neurons. The number of PSA-NCAM/DCX expressing cells in this region decreases markedly as age progresses, suggesting that these cells differentiate or die. Since the piriform cortex receives a major input from the olfactory bulb and participates in olfactory information processing, it is possible that the immature neurons in layer II are affected by manipulations of the olfactory bulb or olfactory learning. It is not known whether these cells can be induced to differentiate and, if so, what would be their fate. In order to address these questions, we have performed unilateral olfactory bulbectomy (OBX) and an olfactory learning paradigm (taste-potentiated odor aversion, TPOA), in young-adult rats and have studied the expression of different mature and immature neuronal markers, as well as the presence of cell death. We have found that 14 h after OBX there was a dramatic decrease in the number of both PSA-NCAM and DCX expressing cells in piriform cortex layer II, whereas that of cells expressing NeuN, a mature neuronal marker, increased. By contrast, the number of cells expressing glutamate decarboxylase, isoform 67 (GAD67), a marker for interneurons, decreased slightly. Additionally, we have not found evidence of numbers of dying cells high enough to justify the disappearance of immature neurons. Analysis of animals subjected to TPOA revealed that this paradigm does not affect PSA-NCAM expressing cells. Our results strongly suggest that OBX can induce the maturation of immature neurons in the piriform cortex layer II and that these cells do not become interneurons. By contrast, these cells do not seem to play a crucial role in olfactory memory.

Place, publisher, year, edition, pages
Elsevier, 2011
Keywords
doublecortin, neuronal differentiation, GAD67, adult neurogenesis, PSA-NCAM, olfactory learning
National Category
Neurosciences
Identifiers
urn:nbn:se:liu:diva-150380 (URN)10.1016/j.neuroscience.2011.03.004 (DOI)000289607000002 ()21382447 (PubMedID)2-s2.0-79953703974 (Scopus ID)
Available from: 2018-08-21 Created: 2018-08-21 Last updated: 2018-08-28Bibliographically approved
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