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  • 1.
    Barr, Gordon A
    et al.
    Department of Anesthesiology and Critical Care Medicine, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania, USA / Department of Developmental Neuroscience, New York State Psychiatric Institute, New York, New York, USA.
    Moriceau, Stephanie
    Department of Zoology, University of Oklahoma, Norman, Oklahoma, USA / Emotional Brain Institute, Nathan Kline Institute, Orangeburg, New York, USA / Child and Adolescent Psychiatry, New York University Langone Medical Center, New York, New York, USA.
    Shionoya, Kiseko
    Department of Zoology, University of Oklahoma, Norman, Oklahoma, USA.
    Muzny, Kyle
    Department of Zoology, University of Oklahoma, Norman, Oklahoma, USA.
    Gao, Puhong
    Department of Developmental Neuroscience, New York State Psychiatric Institute, New York, New York, USA.
    Wang, Shaoning
    Department of Anesthesiology and Critical Care Medicine, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania, USA / Department of Developmental Neuroscience, New York State Psychiatric Institute, New York, New York, USA.
    Sullivan, Regina M
    Department of Zoology, University of Oklahoma, Norman, Oklahoma, USA / Emotional Brain Institute, Nathan Kline Institute, Orangeburg, New York, USA / Child and Adolescent Psychiatry, New York University Langone Medical Center, New York, New York, USA.
    Transitions in infant learning are modulated by dopamine in the amygdala2009In: Nature Neuroscience, ISSN 1097-6256, E-ISSN 1546-1726, Nature Neuroscience, Vol. 12, p. 1367-1369Article in journal (Refereed)
    Abstract [en]

    Behavioral transitions characterize development. Young infant rats paradoxically prefer odors that are paired with shock, but older pups learn aversions. This transition is amygdala and corticosterone dependent. Using microarrays and microdialysis, we found downregulated dopaminergic presynaptic function in the amygdala with preference learning. Corticosterone-injected 8-d-old pups and untreated 12-d-old pups learned aversions and had dopaminergic upregulation in the amygdala. Dopamine injection into the amygdala changed preferences to aversions, whereas dopamine antagonism reinstated preference learning.

  • 2.
    Ericsson, Maria
    et al.
    Linköping University, Department of Physics, Chemistry and Biology, Biology. Linköping University, Faculty of Science & Engineering.
    Henriksen, Rie
    Linköping University, Department of Physics, Chemistry and Biology, Biology. Linköping University, Faculty of Science & Engineering.
    Bélteky, Johan
    Linköping University, Department of Physics, Chemistry and Biology, Biology. Linköping University, Faculty of Science & Engineering.
    Sundman, Ann-Sofie
    Linköping University, Department of Physics, Chemistry and Biology, Biology. Linköping University, Faculty of Science & Engineering.
    Shionoya, Kiseko
    Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Medicine and Health Sciences.
    Jensen, Per
    Linköping University, Department of Physics, Chemistry and Biology, Biology. Linköping University, Faculty of Science & Engineering.
    Long-Term and Transgenerational Effects of Stress Experienced during Different Life Phases in Chickens (Gallus gallus)2016In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 11, no 4, article id e0153879Article in journal (Refereed)
    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.

  • 3.
    Eskilsson, Anna
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Divison of Neurobiology. Linköping University, Faculty of Medicine and Health Sciences.
    Matsuwaki, Takashi
    Linköping University, Department of Clinical and Experimental Medicine, Divison of Neurobiology. Linköping University, Faculty of Medicine and Health Sciences.
    Shionoya, Kiseko
    Linköping University, Department of Clinical and Experimental Medicine, Divison of Neurobiology. Linköping University, Faculty of Medicine and Health Sciences.
    Mirrasekhian, Elahe
    Linköping University, Department of Clinical and Experimental Medicine, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Zajdel, Joanna
    Linköping University, Department of Clinical and Experimental Medicine, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Schwaninger, Markus
    University of Lubeck, Germany.
    Engblom, David
    Linköping University, Department of Clinical and Experimental Medicine, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Blomqvist, Anders
    Linköping University, Department of Clinical and Experimental Medicine, Divison of Neurobiology. Linköping University, Faculty of Medicine and Health Sciences.
    Immune-Induced Fever Is Dependent on Local But Not Generalized Prostaglandin E-2 Synthesis in the Brain2017In: Journal of Neuroscience, ISSN 0270-6474, E-ISSN 1529-2401, Vol. 37, no 19, p. 5035-5044Article in journal (Refereed)
    Abstract [en]

    Fever occurs upon binding of prostaglandin E-2 (PGE(2)) to EP3 receptors in the median preoptic nucleus of the hypothalamus, but the origin of the pyrogenic PGE(2) has not been clearly determined. Here, using mice of both sexes, we examined the role of local versus generalized PGE(2) production in the brain for the febrile response. In wild-type mice and in mice with genetic deletion of the prostaglandin synthesizing enzyme cyclooxygenase-2 in the brain endothelium, generated with an inducible CreER(T2) under the Slco1c1 promoter, PGE(2) levels in the CSF were only weakly related to the magnitude of the febrile response, whereas the PGE(2) synthesizing capacity in the hypothalamus, as reflected in the levels of cyclooxygenase-2 mRNA, showed strong correlation with the immune-induced fever. Histological analysis showed that the deletion of cyclooxygenase-2 in brain endothelial cells occurred preferentially in small-and medium-sized vessels deep in the brain parenchyma, such as in the hypothalamus, whereas larger vessels, and particularly those close to the neocortical surface and in the meninges, were left unaffected, hence leaving PGE(2) synthesis largely intact in major parts of the brain while significantly reducing it in the region critical for the febrile response. Furthermore, injection of a virus vector expressing microsomal prostaglandin E synthase-1 (mPGES-1) into the median preoptic nucleus of fever-refractive mPGES-1 knock-out mice, resulted in a temperature elevation in response to LPS. We conclude that the febrile response is dependent on local release of PGE(2) onto its target neurons and not on the overall PGE(2) production in the brain.

  • 4.
    Gómez-Climent, M. Á
    et al.
    Neurobiology Unit and Program in Basic and Applied Neurosciences, Cell Biology Department, Universitat de València, Spain.
    Hernández-González, S.
    Neurobiology Unit and Program in Basic and Applied Neurosciences, Cell Biology Department, Universitat de València, Spain.
    Shionoya, Kiseko
    CSGA, UMR CNRS 6265, INRA 1354, Université de Bourgogne, 15 rue Picardet, 21000 Dijon, France.
    Belles, M.
    Neurobiology Unit and Program in Basic and Applied Neurosciences, Cell Biology Department, Universitat de València, Spain.
    Alonso-Llosa, G.
    Neurobiology Unit and Program in Basic and Applied Neurosciences, Cell Biology Department, Universitat de València, Spain.
    Datiche, F.
    CSGA, UMR CNRS 6265, INRA 1354, Université de Bourgogne, 15 rue Picardet, 21000 Dijon, France.
    Nacher, J.
    Neurobiology Unit and Program in Basic and Applied Neurosciences, Cell Biology Department, Universitat de València, Spain.
    Olfactory bulbectomy, but not odor conditioned aversion, induces the differentiation of immature neurons in the adult rat piriform cortex2011In: Neuroscience, ISSN 0306-4522, E-ISSN 1873-7544, Vol. 181, no 5, p. 18-27Article in journal (Refereed)
    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.

  • 5.
    Hegoburu, Chloe
    et al.
    Team “Olfaction: From Coding to Memory”, Lyon Neuroscience Research Center, INSERM U1028, CNRS UMR5292, Lyon, France / University Lyon 1, Lyon, France.
    Shionoya, Kiseko
    Team “Olfaction: From Coding to Memory”, Lyon Neuroscience Research Center, INSERM U1028, CNRS UMR5292, Lyon, France / University Lyon 1, Lyon, France.
    Garcia, Samuel
    Team “Olfaction: From Coding to Memory”, Lyon Neuroscience Research Center, INSERM U1028, CNRS UMR5292, Lyon, France / University Lyon 1, Lyon, France.
    Messaoudi, Belkacem
    Team “Olfaction: From Coding to Memory”, Lyon Neuroscience Research Center, INSERM U1028, CNRS UMR5292, Lyon, France / University Lyon 1, Lyon, France.
    Thevenet, Marc
    Team “Olfaction: From Coding to Memory”, Lyon Neuroscience Research Center, INSERM U1028, CNRS UMR5292, Lyon, France / University Lyon 1, Lyon, France.
    Mouly, Anne-Marie
    Team “Olfaction: From Coding to Memory”, Lyon Neuroscience Research Center, INSERM U1028, CNRS UMR5292, Lyon, France / University Lyon 1, Lyon, France.
    The RUB Cage: Respiration–Ultrasonic Vocalizations–Behavior Acquisition Setup for Assessing Emotional Memory in Rats2011In: Frontiers in Behavioral Neuroscience, ISSN 1662-5153, E-ISSN 1662-5153, Vol. 5, p. 1-13, article id 25Article in journal (Refereed)
    Abstract [en]

    In animals, emotional memory is classically assessed through pavlovian fear conditioning in which a neutral novel stimulus (conditioned stimulus) is paired with an aversive unconditioned stimulus. After conditioning, the conditioned stimulus elicits a fear response characterized by a wide range of behavioral and physiological responses. Despite the existence of this large repertoire of responses, freezing behavior is often the sole parameter used for quantifying fear response, thus limiting emotional memory appraisal to this unique index. Interestingly, respiratory changes and ultrasonic vocalizations (USV) can occur during fear response, yet very few studies investigated the link between these different parameters and freezing. The aim of the present study was to design an experimental setup allowing the simultaneous recording of Respiration, USV and Behavior (RUB Cage), and the offline synchronization of the collected data for fine-grain second by second analysis. The setup consisted of a customized plethysmograph for respiration monitoring, equipped with a microphone capturing USV, and with four video cameras for behavior recording. In addition, the bottom of the plethysmograph was equipped with a shock-floor allowing foot-shock delivery, and the top received tubing for odor presentations. Using this experimental setup we first described the characteristics of respiration and USV in different behaviors and emotional states. Then we monitored these parameters during contextual fear conditioning and showed that they bring complementary information about the animal’s anxiety state and the strength of aversive memory. The present setup may be valuable in providing a clearer appraisal of the physiological and behavioral changes that occur during acquisition as well as retrieval of emotional memory.

  • 6.
    Kawai, Mayumi
    et al.
    Department of Medicine, Znstitute of Clinical Endocrinology, Tokyo Women’s Medical College, Tokyo 162, Japan.
    Naruse, Mitsuhide
    Department of Medicine, Znstitute of Clinical Endocrinology, Tokyo Women’s Medical College, Tokyo 162, Japan.
    Yoshimoto, Takanobu
    Department of Medicine, Znstitute of Clinical Endocrinology, Tokyo Women’s Medical College, Tokyo 162, Japan.
    Naruse, Kiyoko
    Department of Medicine, Znstitute of Clinical Endocrinology, Tokyo Women’s Medical College, Tokyo 162, Japan.
    Shionoya, Kiseko
    Department of Medicine, Znstitute of Clinical Endocrinology, Tokyo Women’s Medical College, Tokyo 162, Japan.
    Tanaka, Masami
    Department of Medicine, Znstitute of Clinical Endocrinology, Tokyo Women’s Medical College, Tokyo 162, Japan.
    Morishita, Yoshikazu
    Tokyo Research Laboratories, Kyowa Hakko Kogyo Co., Ltd. Tokyo 194, Japan.
    Matsuda, Yuzuru
    Tokyo Research Laboratories, Kyowa Hakko Kogyo Co., Ltd. Tokyo 194, Japan.
    Demura, Reiko
    Department of Medicine, Znstitute of Clinical Endocrinology, Tokyo Women’s Medical College, Tokyo 162, Japan.
    Demura, Hiroshi
    Department of Medicine, Znstitute of Clinical Endocrinology, Tokyo Women’s Medical College, Tokyo 162, Japan.
    C-type natriuretic peptide as a possible local modulator of aldosterone secretion in bovine adrenal zona glomerulosa1996In: Endocrinology, ISSN 0013-7227, E-ISSN 1945-7170, Vol. 137, no 1, p. 42-46Article in journal (Refereed)
    Abstract [en]

    Although atrial and brain natriuretic peptides are well known to be involved in the regulation of cardiovascular and endocrine functions as circulating hormones, the roles of the C-type natriuretic peptide (CNP) remain unknown. We examined the effects of CNP on the secretion of aldosterone and cyclic nucleotides from bovine adrenal zona glomerulosa cells in culture. CNP produced a dose-dependent increase in the basal secretion of cGMP, with an EC50 of 3.8 x 10(-10)M. CNP significantly inhibited the ACTH-induced increase in aldosterone and cAMP in a dose-related manner, with an IC50 of 3.6 x 10(-10)M. Although ACTH itself did not increase cGMP secretion, the addition of CNP elicited a significant increase in cGMP secretion. The effects of CNP on the basal secretion of cGMP and the ACTH-induced secretion of aldosterone were significantly reversed by a nonpeptide natriuretic peptide receptor antagonist, HS-142-1. CNP immunoreactivity was localized in the zona glomerulosa by immunohistochemical staining. In addition, expression of CNP messenger RNA and natriuretic peptide B receptor messenger RNA was demonstrated by RT-PCR in the zona glomerulosa tissue and cells in culture. These findings suggest that CNP is a local factor regulating ACTH-induced aldosterone secretion through a guanylyl cyclase-cGMP pathway.

  • 7.
    Klawonn, Anna
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Fritz, Michael
    Linköping University, Department of Clinical and Experimental Medicine, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Nilsson, Anna
    Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Medicine and Health Sciences.
    Bonaventura, Jordi
    NIDA, MD USA.
    Shionoya, Kiseko
    Linköping University, Department of Clinical and Experimental Medicine, Divison of Neurobiology. Linköping University, Faculty of Medicine and Health Sciences.
    Mirrasekhian, Elahe
    Linköping University, Department of Clinical and Experimental Medicine, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Karlsson, Urban
    Linköping University, Department of Clinical and Experimental Medicine, Divison of Neurobiology. Linköping University, Faculty of Medicine and Health Sciences.
    Jaarola, Maarit
    Linköping University, Department of Clinical and Experimental Medicine, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Granseth, Björn
    Linköping University, Department of Clinical and Experimental Medicine, Divison of Neurobiology. Linköping University, Faculty of Medicine and Health Sciences.
    Blomqvist, Anders
    Linköping University, Department of Clinical and Experimental Medicine, Divison of Neurobiology. Linköping University, Faculty of Medicine and Health Sciences.
    Michaelides, Michael
    NIDA, MD USA; Johns Hopkins Sch Med, MD USA.
    Engblom, David
    Linköping University, Department of Clinical and Experimental Medicine, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Motivational valence is determined by striatal melanocortin 4 receptors2018In: Journal of Clinical Investigation, ISSN 0021-9738, E-ISSN 1558-8238, Vol. 128, no 7, p. 3160-3170Article in journal (Refereed)
    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.

  • 8.
    Matsuwaki, Takashi
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Divison of Neurobiology. Linköping University, Faculty of Medicine and Health Sciences. University of Tokyo, Japan.
    Shionoya, Kiseko
    Linköping University, Department of Clinical and Experimental Medicine, Divison of Neurobiology. Linköping University, Faculty of Medicine and Health Sciences.
    Ihnatko, Robert
    Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology and Molecular Medicine. Linköping University, Faculty of Medicine and Health Sciences.
    Eskilsson, Anna
    Linköping University, Department of Clinical and Experimental Medicine, Divison of Neurobiology. Linköping University, Faculty of Medicine and Health Sciences.
    Kakuta, Shigeru
    University of Tokyo, Japan.
    Dufour, Sylvie
    CNRS, France.
    Schwaninger, Markus
    University of Lubeck, Germany.
    Waisman, Ari
    Johannes Gutenberg University of Mainz, Germany.
    Mueller, Werner
    University of Manchester, England.
    Pinteaux, Emmanuel
    University of Manchester, England.
    Engblom, David
    Linköping University, Department of Clinical and Experimental Medicine, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Blomqvist, Anders
    Linköping University, Department of Clinical and Experimental Medicine, Divison of Neurobiology. Linköping University, Faculty of Medicine and Health Sciences.
    Involvement of interleukin-1 type 1 receptors in lipopolysaccharide-induced sickness responses2017In: Brain, behavior, and immunity, ISSN 0889-1591, E-ISSN 1090-2139, Vol. 66, p. 165-176Article in journal (Refereed)
    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. 

  • 9.
    Mirrasekhian, Elahe
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Nilsson, Johan L. Å.
    Division of Clinical Chemistry and Pharmacology, Department of Laboratory Medicine, Lund University, Lund, Sweden.
    Shionoya, Kiseko
    Linköping University, Department of Clinical and Experimental Medicine, Divison of Neurobiology. Linköping University, Faculty of Medicine and Health Sciences.
    Blomgren, Anders
    Division of Clinical Chemistry and Pharmacology, Department of Laboratory Medicine, Lund University, Lund, Sweden.
    Zygmunt, Peter M.
    Division of Clinical Chemistry and Pharmacology, Department of Laboratory Medicine, Lund University, S-221 85 Lund, Sweden.
    Engblom, David
    Linköping University, Department of Clinical and Experimental Medicine, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Högestätt, Edward D.
    Division of Clinical Chemistry and Pharmacology, Department of Laboratory Medicine, Lund University, Lund, Sweden.
    Blomqvist, Anders
    Linköping University, Department of Clinical and Experimental Medicine, Divison of Neurobiology. Linköping University, Faculty of Medicine and Health Sciences.
    The antipyretic effect of paracetamol occurs independent of transient receptor potential ankyrin 1–mediated hypothermia and is associated with prostaglandin inhibition in the brain2018In: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860Article in journal (Refereed)
    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.

  • 10.
    Moriceau, Stephanie
    et al.
    Emotional Brain Institute, Nathan Kline Institute, Orangeburg, New York, USA, / Child and Adolescent Psychiatry, Child Study Center, New York University Langone Medical Center, New York, New York, USA, Department of Zoology, University of Oklahoma, Norman, Oklahoma, USA.
    Shionoya, Kiseko
    Department of Zoology, University of Oklahoma, Norman, Oklahoma, USA / Laboratory Neurosciences Sensorielles, Centre National de la Recherche Scientifique, Universite Lyon, 69007 Lyon, France.
    Jakubs, Katherine
    Department of Zoology, University of Oklahoma, Norman, Oklahoma, USA / National Institutes of Health, Bethesda, Maryland, USA.
    Sullivan, Regina M.
    Emotional Brain Institute, Nathan Kline Institute, Orangeburg, New York, USA / Child and Adolescent Psychiatry, Child Study Center, New York University Langone Medical Center, New York, New York, USA / New York University Center for Neural Science, New York, New York, USA / Department of Zoology, University of Oklahoma, Norman, Oklahoma, USA.
    Early-Life Stress Disrupts Attachment Learning: The Role of Amygdala Corticosterone, Locus Ceruleus Corticotropin Releasing Hormone, and Olfactory Bulb Norepinephrine2009In: Journal of Neuroscience, ISSN 0270-6474, E-ISSN 1529-2401, Vol. 29, no 50, p. 15745-15755Article in journal (Refereed)
    Abstract [en]

    Infant rats require maternal odor learning to guide pups’ proximity-seeking of the mother and nursing. Maternal odor learning occurs using a simple learning circuit including robust olfactory bulb norepinephrine (NE), release from the locus ceruleus (LC), and amygdala suppression by low corticosterone (CORT). Early-life stress increases NE but also CORT, and we questioned whether early-life stress disrupted attachment learning and its neural correlates [2-deoxyglucose (2-DG) autoradiography]. Neonatal rats were normally reared or stressed-reared during the first 6 d of life by providing the mother with insufficient bedding for nest building and were odor–0.5 mA shock conditioned at 7 d old. Normally reared paired pups exhibited typical odor approach learning and associated olfactory bulb enhanced 2-DG uptake. However, stressed-reared pups showed odor avoidance learning and both olfactory bulb and amygdala 2-DG uptake enhancement. Furthermore, stressed-reared pups had elevated CORT levels, and systemic CORT antagonist injection reestablished the age-appropriate odor-preference learning, enhanced olfactory bulb, and attenuated amygdala 2-DG. We also assessed the neural mechanism for stressed-reared pups’ abnormal behavior in a more controlled environment by injecting normally reared pups with CORT. This was sufficient to produce odor aversion, as well as dual amygdala and olfactory bulb enhanced 2-DG uptake. Moreover, we assessed a unique cascade of neural events for the aberrant effects of stress rearing: the amygdala–LC–olfactory bulb pathway. Intra-amygdala CORT or intra-LC corticotropin releasing hormone (CRH) infusion supported aversion learning with intra-LC CRH infusion associated with increased olfactory bulb NE (microdialysis). These results suggest that early-life stress disturbs attachment behavior via a unique cascade of events (amygdala–LC–olfactory bulb).

  • 11.
    Moriceau, Stephanie
    et al.
    Zoology Department, University of Oklahoma, Norman, USA.
    Shionoya, Kiseko
    Zoology Department, University of Oklahoma, Norman, USA.
    Sullivan, Regina M.
    Zoology Department, University of Oklahoma, Norman, USA.
    Concurrent Neonatal Activation Of The Amygdala-fear Circuit And The Attachment Circuit During Infancy2007Conference paper (Refereed)
    Abstract [en]

    Infant altricial species learn to prefer stimuli paired with pain, presumably due to the importance of learning to prefer the caregiver regardless of the qual ity of care. This attenuated avoidance/fear learning appears due to low corticosterone (CORT), which keeps the amygdala ‘‘dormant’’. Indeed, simply increasing CORT permits amygdala plasticity and fear conditioning. Here we assess whether CORT also activates the locus coeruleus (LC) and increases NE via amygdala CRF efferents to the LC. In all experiments, PN7–8 pups received 11 pairings of odor-0.5 mA shock and were tested the next day for an odor preference/aversion (Y-maze). 14C 2-DG was used for neural assessment during conditioning. In Experiment 1, we found that the CORT induced odor aversion was correlated with olfactory bulb activation. Since this neural change is usually dependent upon increased NE and limited to neonates, we next assessed the pathway from the amygdala to the LC. In Experiment 2, we directly infused CORT into the lateral amygdala that activates the CRF efferents to the LC and an odor aversion was again obtained. In Experiment 3, we infused CRF directly into the LC, which produced an odor aversion and an increase in olfactory bulb NE (microdialysis). Pups with control LC vehicle infusions continued to acquire the age characteristic shock-induced odor preference. These results suggested that early activation of the amygdala dependent fear system can be precociously induce in neonates, although this is done in concert with the neonatal NE olfactory bulb learning system. [RMS Funding NSF IBN0117234, NICHD HD33402, OCAST]

  • 12.
    Raineki, Charlis
    et al.
    Emotional Brain Institute, Nathan Kline Institute for Psychiatric Research, Child and Adolescent Psychiatry, Child Study Center, New York University Langone Medical Center, Orangeburg, New York 10962, USA / Department of Zoology, University of Oklahoma, Norman, Oklahoma 73019, USA / Department of Zoology, University of Oklahoma, Norman, Oklahoma 73019, USA .
    Shionoya, Kiseko
    Department of Zoology, University of Oklahoma, Norman, Oklahoma 73019, USA.
    Sander, Kristin
    Department of Zoology, University of Oklahoma, Norman, Oklahoma 73019, USA.
    Sullivan, Regina M.
    Emotional Brain Institute, Nathan Kline Institute for Psychiatric Research, Child and Adolescent Psychiatry, Child Study Center, New York University Langone Medical Center, Orangeburg, New York 10962, USA / Department of Zoology, University of Oklahoma, Norman, Oklahoma 73019, USA / Department of Zoology, University of Oklahoma, Norman, Oklahoma 73019, USA .
    Ontogeny of odor-LiCl vs. odor-shock learning: Similar behaviors but divergent ages of functional amygdala emergence2009In: Learning & memory (Cold Spring Harbor, N.Y.), ISSN 1072-0502, E-ISSN 1549-5485, Vol. 16, no 2, p. 114-121Article in journal (Refereed)
    Abstract [en]

    Both odor-preference and odor-aversion learning occur in perinatal pups before the maturation of brain structures that support this learning in adults. To characterize the development of odor learning, we compared three learning paradigms: (1) odor-LiCl (0.3M; 1% body weight, ip) and (2) odor-1.2-mA shock (hindlimb, 1sec)ᅵboth of which consistently produce odor-aversion learning throughout life and (3) odor-0.5-mA shock, which produces an odor preference in early life but an odor avoidance as pups mature. Pups were trained at postnatal day (PN) 7ᅵ8, 12ᅵ13, or 23ᅵ24, using odor-LiCl and two odor-shock conditioning paradigms of odor-0.5-mA shock and odor-1.2-mA shock. Here we show that in the youngest pups (PN7ᅵ8), odor-preference learning was associated with activity in the anterior piriform (olfactory) cortex, while odor-aversion learning was associated with activity in the posterior piriform cortex. At PN12ᅵ13, when all conditioning paradigms produced an odor aversion, the odor-0.5-mA shock, odor-1.2-mA shock, and odor-LiCl all continued producing learning-associated changes in the posterior piriform cortex. However, only odor-0.5-mA shock induced learning-associated changes within the basolateral amygdala. At weaning (PN23ᅵ24), all learning paradigms produced learning-associated changes in the posterior piriform cortex and basolateral amygdala complex. These results suggest at least two basic principles of the development of the neurobiology of learning: (1) Learning that appears similar throughout development can be supported by neural systems showing very robust developmental changes, and (2) the emergence of amygdala function depends on the learning protocol and reinforcement condition being assessed.

  • 13.
    Rincon-Cortes, Millie
    et al.
    Nathan S Kline Institute Psychiat Research, NY 10962 USA; NYU, NY 10016 USA; NYU, NY 10016 USA.
    Barr, Gordon A.
    Childrens Hospital Philadelphia, PA 19104 USA; University of Penn, PA 19104 USA.
    Marie Mouly, Anne
    University of Lyon 1, France.
    Shionoya, Kiseko
    Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Health Sciences.
    Nunez, Bestina S.
    Nathan S Kline Institute Psychiat Research, NY 10962 USA.
    Sullivan, Regina M.
    Nathan S Kline Institute Psychiat Research, NY 10962 USA; NYU, NY 10016 USA; NYU, NY 10016 USA.
    Enduring good memories of infant trauma: Rescue of adult neurobehavioral deficits via amygdala serotonin and corticosterone interaction2015In: 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)
    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.

  • 14.
    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 memory2009In: Neurobiology of Learning and Memory, ISSN 1074-7427, E-ISSN 1095-9564, Vol. 92, no 4, p. 590-596Article in journal (Refereed)
    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.

  • 15.
    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 rats2013In: Frontiers in Behavioral Neuroscience, ISSN 1662-5153, E-ISSN 1662-5153, Vol. 7, article id 128Article in journal (Refereed)
    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.

  • 16.
    Shionoya, Kiseko
    et al.
    Neurobehavioral Institute and Department of Zoology, University of Oklahoma, 730 Van Vleet Oval, Norman, OK 73019, USA.
    Moriceau, Stephanie
    Neurobehavioral Institute and Department of Zoology, University of Oklahoma, 730 Van Vleet Oval, Norman, OK 73019, USA.
    Bradstock, Peter
    Neurobehavioral Institute and Department of Zoology, University of Oklahoma, 730 Van Vleet Oval, Norman, OK 73019, USA.
    Sullivan, Regina M.
    Neurobehavioral Institute and Department of Zoology, University of Oklahoma, 730 Van Vleet Oval, Norman, OK 73019, USA.
    Maternal attenuation of hypothalamic paraventricular nucleus norepinephrine switches avoidance learning to preference learning in preweanling rat pups2007In: Hormones and Behavior, ISSN 0018-506X, E-ISSN 1095-6867, Vol. 52, no 3, p. 391-400Article in journal (Refereed)
    Abstract [en]

    Infant rats learn to prefer stimuli paired with pain, presumably due to the importance of learning to prefer the caregiver to receive protection and food. With maturity, a more ‘adult-like’ learning system emerges that includes the amygdala and avoidance/fear learning. The attachment and ‘adult-like’ systems appear to co-exist in older pups with maternal presence engaging the attachment system by lowering corticosterone (CORT). Specifically, odor–shock conditioning (11 odor–0.5 mA shock trials) in 12-day-old pups results in an odor aversion, although an odor preference is learned if the mother is present during conditioning. Here, we propose a mechanism to explain pups ability to ‘switch’ between the dual learning systems by exploring the effect of maternal presence on hypothalamic paraventricular nucleus (PVN) neural activity, norepinephrine (NE) levels and learning. Maternal presence attenuates both PVN neural activity and PVN NE levels during odor–shock conditioning. Intra-PVN NE receptor antagonist infusion blocked the odor aversion learning with maternal absence, while intra-PVN NE receptor agonist infusion permitted odor aversion learning with maternal presence. These data suggest maternal control over pup learning acts through attenuation of PVN NE to reduce the CORT required for pup odor aversion learning. Moreover, these data also represent pups’ continued maternal dependence for nursing, while enabling aversion learning outside the nest to prepare for pups future independent living.

  • 17.
    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 learning2006In: Learning & memory (Cold Spring Harbor, N.Y.), ISSN 1072-0502, E-ISSN 1549-5485, Vol. 13, no 6, p. 801-808Article in journal (Refereed)
    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.

  • 18.
    Shionoya, Kiseko
    et al.
    NEC CorporationTokyo, Japan.
    Saito, Atsushi
    NEC CorporationTokyo, Japan.
    Immobilized enzyme film, protein immobilized film and process for forming the same: Patent abstracts. Patent No. 53567571995In: Biotechnology Advances, ISSN 0734-9750, E-ISSN 1873-1899, Vol. 13, no 2, p. 300-300Article in journal (Refereed)
    Abstract [en]

    Disclosed are an immobilized enzyme film, characterized in that said film is formed using an enzyme solution prepared by adding 1 to 3 parts by weight of a 50 to 100 wt % water-soluble crosslinking agent having at least two epoxy groups in the molecule and 1 to 3 parts by weight of a 1 to 2 wt % glutaraldehyde to 1 to 3 parts by weight of a 10 to 50 wt % aqueous protein solution containing an enzyme, and a process for forming the same on an ion-sensitive field effect transistor. The thus formed immobilized enzyme film is of an uniform thickness and stable by virtue of its increased hydrophilicity and higher elasticity, whereby deactivation of the enzyme to be caused by the shrinkage of the film can be prevented.

  • 19.
    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 Modulation2009In: Neural Plasticity, ISSN 2090-5904, E-ISSN 1687-5443, Vol. 2009, article id 754014Article in journal (Refereed)
    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.

  • 20.
    Sullivan, R. M.
    et al.
    Emotional Brain Institute, Nathan Kline Institute, Orangeburg, NY, USA.
    Shionoya, Kiseko
    Lyon Neuroscience Research Center, INSERM U1028; CNRS UMR5292; Université Lyon1, Lyon, France.
    Boulanger Bertolus, J.
    Lyon Neuroscience Research Center, INSERM U1028; CNRS UMR5292; Université Lyon1, Lyon, France.
    Ahers, J.
    Emotional Brain Institute, Nathan Kline Institute, Orangeburg, NY, USA.
    Londen, E.
    Emotional Brain Institute, Nathan Kline Institute, Orangeburg, NY, USA.
    Hegoburu, C.
    Lyon Neuroscience Research Center, INSERM U1028; CNRS UMR5292; Université Lyon1, Lyon, France.
    Sullivan-Wilson, T.
    Emotional Brain Institute, Nathan Kline Institute, Orangeburg, NY, USA.
    Rousselot, J.
    Lyon Neuroscience Research Center, INSERM U1028; CNRS UMR5292; Université Lyon1, Lyon, France.
    Brown, B. L.
    Dept. of Psychology, Queens College, New-York, USA.
    Doyère, V.
    Neurobiology of Executive Function, Center of Neuroscience Paris-Sud, CNRS-UMR8195, Paris, France.
    Mouly, A-M.
    Lyon Neuroscience Research Center, INSERM U1028; CNRS UMR5292; Université Lyon1, Lyon, France.
    Ontogenesis Of Time Interval Encoding In Odor Fear Conditioning2012In: Developmental Psychobiology, ISSN 0012-1630, E-ISSN 1098-2302, Vol. 54, no 7, p. 768-768Article in journal (Refereed)
    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.

  • 21.
    Sullivan, Regina M.
    et al.
    Emotional Brain Institute, Nathan S. Kline Institute for Psychiatric Research, Child and Adolescent Psychiatry, New York University Langone Medical Center, New York, NY, USA.
    Moriceau, Stephanie
    Emotional Brain Institute, Nathan S. Kline Institute for Psychiatric Research, Child and Adolescent Psychiatry, New York University Langone Medical Center, New York, NY, USA.
    Roth, Tania
    Department of Psychology, University of Delaware, Newark, DE, USA.
    Shionoya, Kiseko
    Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Medicine and Health Sciences.
    Developmental Neurobiology of Olfactory Preference and Avoidance Learning2014In: 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.

  • 22.
    Yoshimoto, Takanobu
    et al.
    Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College, Tokyo, 162, Japan.
    Naruse, Mitsuhide
    Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College, Tokyo, 162, Japan.
    Naruse, Kiyoko
    Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College, Tokyo, 162, Japan.
    Shionoya, Kiseko
    Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College, Tokyo, 162, Japan.
    Tanabe, Akiyo
    Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College, Tokyo, 162, Japan.
    Tanaka, Masami
    Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College, Tokyo, 162, Japan.
    Hagiwara, Hiromi
    Department of Biological Sciences, Tokyo Institute of Technology, Yokohama, 227, Japan.
    Hirose, Shigehsia
    Department of Biological Sciences, Tokyo Institute of Technology, Yokohama, 227, Japan.
    Muraki, Takamura
    Department of Pharmacology, Tokyo Women’s Medical College, Tokyo 162, Japan.
    Demura, Hiroshi
    Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College, Tokyo, 162, Japan.
    Differential Gene Expression of Vascular Natriuretic Peptide Receptor Subtype in Artery and Vein1995In: Biochemical and Biophysical Research Communications - BBRC, ISSN 0006-291X, E-ISSN 1090-2104, Vol. 216, no 2, p. 535-539Article in journal (Refereed)
    Abstract [en]

    Although the vasorelaxation by natriuretic peptide (NP) is much less potent in the vein than in the artery, mechanism underlying the phenomenon remains unknown. Since NP receptor consists of three subtypes with different functions, we determined the mRNA level of each NP receptor subtype in the artery and vein by ribonuclease protection assay. In the aorta, NP-A receptor related to the biological action of NP was the predominant form. By contrast, NP-C receptor related mainly to the clearance of NP was the predominant form in the inferior vena cava: NP-C mRNA level was about two fold higher than in the aorta, while both NP-A and NP-B receptor mRNA levels were about half of that in the aorta. These results provide the molecular basis for the different biological response to NP in the artery and vein. Differential gene expression of NP receptor subtype could be an important determinant of the biological actions of NP.

  • 23.
    Yoshimoto, Takanobu
    et al.
    Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College, Tokyo 162, Japan.
    Naruse, Mitsuhide
    Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College, Tokyo 162, Japan.
    Naruse, Kiyoko
    Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College, Tokyo 162, Japan.
    Tanabe, Akiyo
    Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College, Tokyo 162, Japan.
    Tanaka, Masami
    Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College, Tokyo 162, Japan.
    Arai, Keiko
    Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College, Tokyo 162, Japan.
    Shionoya, Kiseko
    Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College, Tokyo 162, Japan.
    Hagiwara, Hiromi
    Department of Biological Science, Tokyo Institute of Technology, Yokohama 227, Japan .
    Hirose, Shigehisa
    Department of Biological Science, Tokyo Institute of Technology, Yokohama 227, Japan .
    Demura, Hiroshi
    Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College, Tokyo 162, Japan.
    Gene Expression of Vascular Natriutretic Peptide Receptor Type A is Upregulated in Hypertensive Rats1996In: Japanese Heart Journal, ISSN 0021-4868, E-ISSN 1348-673X, Vol. 37, no 4, p. 560-560Article in journal (Refereed)
    Abstract [en]

    Not Available.

  • 24.
    Yoshimoto, Takanoubu
    et al.
    Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College, Tokyo, 162, Japan.
    Naruse, Mitsuhide
    Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College, Tokyo, 162, Japan.
    Naruse, Kiyoko
    Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College, Tokyo, 162, Japan.
    Shionoya, Kiseko
    Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College, Tokyo, 162, Japan.
    Tanaka, Masami
    Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College, Tokyo, 162, Japan.
    Tanabe, Akiyo
    Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College, Tokyo, 162, Japan.
    Hagiwara, Hiromi
    Department of Biological Sciences, Tokyo Institute of Technology, Yokohama, 227, Japan.
    Hirose, Shigehisa
    Department of Biological Sciences, Tokyo Institute of Technology, Yokohama 227, Japan.
    Muraki, Takamura
    Department of Pharmacology, Tokyo Women’s Medical College, Tokyo 162, Japan.
    Demura, Hiroshi
    Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College, Tokyo, 162, Japan.
    Angiotensin II-dependent down-regulation of vascular natriuretic peptide type C receptor gene expression in hypertensive rats1996In: Endocrinology, ISSN 0013-7227, E-ISSN 1945-7170, Vol. 137, no 3, p. 1102-1107Article in journal (Refereed)
    Abstract [en]

    Biological actions of natriuretic peptide (NP) are determined by the condition of the receptor as well as that of the hormone. Although we previously demonstrated in hypertensive rats the up-regulation of NP-A receptor that mediates various biological actions of NPs, the pathophysiologic significance of NP-C receptor, another subtype thought to be related to clearance of NPs and possibly to biological actions, remains unknown. In the present study, we determined NP-C receptor messenger RNA (mRNA) level in the aortic tissue of stroke-prone spontaneously hypertensive rats (SHR-SP/Izm) and in cultured aortic smooth muscle cells by ribonuclease protection assay. The aortic NP-C receptor mRNA level in SHR-SP/Izm was significantly lower than that in the control WKY/Izm. Oral administration of an angiotensin (Ang) II receptor (AT1) antagonist, TCV-116, but not a calcium channel blocker, manidipine, reversed the down-regulated NP-C receptor mRNA in SHR-SP/Izm to the level in WKY/Izm, whereas the latter was more potent in decreasing the blood pressure. In cultured aortic smooth muscle cells, the NP-C receptor was the predominant subtype. Ang II decreased the NP-C receptor mRNA level in a dose-dependent manner, but this effect was reversed by an AT1 antagonist, CV-11974. Neither the NP-A nor NP-B receptor mRNA level was altered by Ang II. These findings indicate that vascular NP-C receptor is down- regulated via Ang-II-mediated mechanism in SHR-SP/Izm. The phenomenon, together with the up-regulation of the NP-A receptor, may play an important role in counteracting hypertension by enhancing the action of NPs.

  • 25.
    Zajdel, Joanna
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Zager, Adriano
    Linköping University, Department of Clinical and Experimental Medicine, Divison of Neurobiology. Linköping University, Faculty of Medicine and Health Sciences.
    Blomqvist, Anders
    Linköping University, Department of Clinical and Experimental Medicine, Divison of Neurobiology. Linköping University, Faculty of Medicine and Health Sciences.
    Engblom, David
    Linköping University, Department of Clinical and Experimental Medicine, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Shionoya, Kiseko
    Linköping University, Department of Clinical and Experimental Medicine, Divison of Neurobiology. Linköping University, Faculty of Medicine and Health Sciences.
    Acute maternal separation potentiates the gene expression and corticosterone response induced by inflammation2019In: Brain, behavior, and immunity, ISSN 0889-1591, E-ISSN 1090-2139, Vol. 77, p. 141-149Article in journal (Refereed)
    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.

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