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      Investigating the Effects of Maternal Separation on Hypothalamic-Pituitary-Adrenal Axis and Glucose Homeostasis under Chronic Social Defeat Stress in Young Adult Male Rat Offspring

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          Abstract

          Introduction: Given the suggested metabolic regulatory effects of stress-responsive genes and based on the impacts of early-life stress on HPA axis development, this study aimed to characterize the maternal separation (MS) impact on the communication between glucose metabolism and HPA axis dysregulations under chronic social defeat stress (CSDS). Methods: During the first 2 weeks of life, male Wistar rats were either exposed to MS or left undisturbed with their mothers (Std). Starting on postnatal day 50, the animals of each group were either left undisturbed in the standard group housing (Con) or underwent CSDS for 3 weeks. There were four groups ( n = 10/group): Std-Con, MS-Con, Std-CSDS, and MS-CSDS. Results: Early and/or adult life adversity reduced β-cell number, muscular FK506-binding protein 51 (FKBP51) content, and BMI in adulthood. The reduction of β-cell number and BMI in the MS-CSDS rats were more profound than MS-Con group. CSDS either alone or in combination with MS reduced locomotor activity and increased and decreased corticotropin-releasing factor type 1 receptor (CRFR1) content, respectively, in hypothalamus and pancreas. Although, under CSDS, MS intensified HPA axis overactivity and reduced isolated islets’ insulin secretion, it could promote resilience to depression symptoms. No differences were observed in hypothalamic Fkbp5 gene DNA methylation and glucose tolerance among groups. Conclusion: MS exacerbated HPA axis overactivity and the endocrine pancreas dysfunctions under CSDS. The intensified corticosterone secretion and the diminished content of pancreatic CRFR1 protein could be involved in the reduced β-cell number and islets’ insulin secretion under CSDS. The decreased muscular FKBP51 content might be a homeostatic response to slow down insulin resistance development under chronic stress.

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          A Rapid and Sensitive Method for the Quantitation of Microgram Quantities of Protein Utilizing the Principle of Protein-Dye Binding

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            Molecular adaptations underlying susceptibility and resistance to social defeat in brain reward regions.

            While stressful life events are an important cause of psychopathology, most individuals exposed to adversity maintain normal psychological functioning. The molecular mechanisms underlying such resilience are poorly understood. Here, we demonstrate that an inbred population of mice subjected to social defeat can be separated into susceptible and unsusceptible subpopulations that differ along several behavioral and physiological domains. By a combination of molecular and electrophysiological techniques, we identify signature adaptations within the mesolimbic dopamine circuit that are uniquely associated with vulnerability or insusceptibility. We show that molecular recapitulations of three prototypical adaptations associated with the unsusceptible phenotype are each sufficient to promote resistant behavior. Our results validate a multidisciplinary approach to examine the neurobiological mechanisms of variations in stress resistance, and illustrate the importance of plasticity within the brain's reward circuits in actively maintaining an emotional homeostasis.
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              Characterization of a 41-residue ovine hypothalamic peptide that stimulates secretion of corticotropin and beta-endorphin

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                Author and article information

                Journal
                NEN
                Neuroendocrinology
                10.1159/issn.0028-3835
                Neuroendocrinology
                Neuroendocrinology
                S. Karger AG
                0028-3835
                1423-0194
                2023
                March 2023
                09 September 2022
                : 113
                : 3
                : 361-380
                Affiliations
                [_a] aNeurophysiology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran
                [_b] bDepartment of Physiology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
                [_c] cDepartment of Biology and Anatomical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran
                [_d] dDepartment of Biotechnology, School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
                [_e] eCellular and Molecular Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran
                Author information
                https://orcid.org/0000-0002-6704-6279
                https://orcid.org/0000-0001-5816-775X
                https://orcid.org/0000-0002-5086-4208
                Article
                526989 Neuroendocrinology 2023;113:361–379
                10.1159/000526989
                36088912
                f6402be1-6840-4d30-8041-4be148e29e5e
                © 2022 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.

                History
                : 29 March 2022
                : 05 September 2022
                Page count
                Figures: 7, Tables: 4, Pages: 19
                Funding
                This work has been supported financially by the Neurophysiology Research Center, Shahid Beheshti University of Medical Sciences (Grant No. 16909).
                Categories
                Research Article

                Medicine
                Social defeat,FK506-binding protein 51,Corticotropin-releasing factor type 1 receptor,Insulin secretion,Maternal separation

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