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      Paternal deprivation affects the functional maturation of corticotropin-releasing hormone (CRH)- and calbindin-D28k-expressing neurons in the bed nucleus of the stria terminalis (BNST) of the biparental Octodon degus

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          Abstract

          While the critical role of maternal care on the development of brain and behavior of the offspring has been extensively studied, our knowledge about the importance of paternal care for brain development of his offspring is still comparatively scarce. The aim of this study in the biparental caviomorph rodent Octodon degus was to analyze the impact of paternal care on the development of corticotropin-releasing hormone (CRH)-expressing neurons in the bed nucleus of the stria terminalis (BNST) and hypothalamic paraventricular nucleus (PVN). Both brain areas are key players in neuronal circuits that regulate hypothalamic–pituitary–adrenal axis (HPA) activity. At the age of postnatal day (PND) 21, we found that paternal deprivation resulted in a decreased density of CRH-containing neurons in the medial, but not in the lateral BNST, whereas no changes were observed in the PVN. These deprivation-induced changes were still prominent in adulthood. At PND 21, the density of Ca-binding protein calbindin D28K (CaBP-D28K)-expressing neurons was specifically increased in the medial, but not lateral BNST of father-deprived animals. In contrast, adult father-deprived animals show significantly decreased density of CaBP-D28K-expressing neurons in the lateral, but not medial BNST. Taken together, these results may have important implications for our understanding of the experience-driven development of neural circuits that regulate HPA activity mediating acute responses to stress and chronic anxiety.

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          Most cited references40

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          Emotion: clues from the brain.

          J E LeDoux (1995)
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            Role of the bed nucleus of the stria terminalis versus the amygdala in fear, stress, and anxiety.

            The bed nucleus of the stria terminalis is a limbic forebrain structure that receives heavy projections from, among other areas, the basolateral amygdala, and projects in turn to hypothalamic and brainstem target areas that mediate many of the autonomic and behavioral responses to aversive or threatening stimuli. Despite its strategic anatomical position, initial attempts to implicate the bed nucleus of the stria terminalis in conditioned fear were largely unsuccessful. Recent studies have shown, however, that the bed nucleus of the stria terminalis does participate in certain types of anxiety and stress responses. In this work, we review these findings and suggest from the emerging pattern of evidence that, although the bed nucleus of the stria terminalis may not be necessary for rapid-onset, short-duration behaviors which occur in response to specific threats, the bed nucleus of the stria terminalis may mediate slower-onset, longer-lasting responses that frequently accompany sustained threats, and that may persist even after threat termination.
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              From normal fear to pathological anxiety.

              In this article the authors address how pathological anxiety may develop from adaptive fear states. Fear responses (e.g., freezing, startle, heart rate and blood pressure changes, and increased vigilance) are functionally adaptive behavioral and perceptual responses elicited during danger to facilitate appropriate defensive responses that can reduce danger or injury (e.g., escape and avoidance). Fear is a central motive state of action tendencies subserved by fear circuits, with the amygdala playing a central role. Pathological anxiety is conceptualized as an exaggerated fear state in which hyperexcitability of fear circuits that include the amygdala and extended amygdala (i.e., bed nucleus of the stria terminalis) is expressed as hypervigilance and increased behavioral responsivity to fearful stimuli. Reduced thresholds for activation and hyperexcitability in fear circuits develop through sensitization- or kindling-like processes that involve neuropeptides, hormones, and other proteins. Hyperexcitability in fear circuits is expressed as pathological anxiety that is manifested in the various anxiety disorders.
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                Author and article information

                Contributors
                +39-1-6755001 , +39-1-6755002 , katharina.braun@ovgu.de
                Journal
                Brain Struct Funct
                Brain Struct Funct
                Brain Structure & Function
                Springer Berlin Heidelberg (Berlin/Heidelberg )
                1863-2653
                1863-2661
                3 August 2013
                3 August 2013
                2014
                : 219
                : 6
                : 1983-1990
                Affiliations
                [ ]Institute of Forensic Medicine, Medical University of Gdansk, ul. Sklodowskiej-Curie 3a, 80-210 Gdansk, Poland
                [ ]Department of Neuroscience, Center for the Brain Basis of Cognition, Georgetown University, Washington DC, 20007 USA
                [ ]Department of Obstetrics and Gynecology, University of Washington, Seattle, WA 98195 USA
                [ ]Institute for Biology, Human Biology, University of Leipzig, Talstraße 33, 04103 Leipzig, Germany
                [ ]Department of Zoology/Developmental Neurobiology, Institute of Biology, Otto von Guericke University, Leipziger Straße 44, 39120 Magdeburg, Germany
                [ ]Project Group Epigenetics and Structural Plasticity, Institute of Biology, Otto von Guericke University, 39120 Magdeburg, Germany
                [ ]Center for Behavioral Brain Sciences (CBBS), Magdeburg, Germany
                Article
                617
                10.1007/s00429-013-0617-4
                4223576
                23913254
                d983e4ae-f4c7-43cc-805f-326b8116bb70
                © The Author(s) 2013

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.

                History
                : 10 May 2013
                : 23 July 2013
                Categories
                Original Article
                Custom metadata
                © Springer-Verlag Berlin Heidelberg 2014

                Neurology
                parental behavior,development,corticotropin-releasing factor,quantitative immunocytochemistry

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