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Chronic exposure to stressful experiences impairs synaptic plasticity. Previous studies have shown that the spine densities of pyramidal neurons, the turnover of mushroom-type spines, and the excitatory–inhibitory balance in the primary somatosensory cortex (S1) are modulated by stress. Trans-synaptic cell adhesion molecules (CAMs) are implicated in stress-induced synaptic deficits. However, it remains unknown whether stress dysregulates CAMs in S1 and thereby impairs synaptic plasticity. In this study, we applied the early-life stress (ELS), chronic social defeat stress (CSDS), and chronic restraint stress paradigms and measured the mRNA levels of nectin1 in S1 of wild-type and conditional forebrain corticotropin-releasing hormone receptor 1 type (CRHR1) conditional knockout mice. We found that ELS increased nectin1 mRNA levels in S1 in adult but not adolescent mice. Moreover, CSDS increased the nectin1 mRNA levels in S1 in adult mice via the CRH-CRHR1 system. Our findings suggest that S1 is vulnerable to repeated stress exposures at some life stages, and dysregulated nectin1 expression may underlie stress-induced structural and functional abnormalities in S1.


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Effects of chronic stress on nectin1 levels in the mouse primary somatosensory cortex

Show Author's information Xue Xu1,2Xiao-Dong Wang1,2( )
Department of Neurobiology and Department of Psychiatryof Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou 310058, China
NHC and CAMS Key Laboratory of Medical Neurobiology, MOE Frontier Science Center for Brain Research and Brain-Machine Integration, School of Brain Science and Brain Medicine, Zhejiang University, Hangzhou 310058, China

Abstract

Chronic exposure to stressful experiences impairs synaptic plasticity. Previous studies have shown that the spine densities of pyramidal neurons, the turnover of mushroom-type spines, and the excitatory–inhibitory balance in the primary somatosensory cortex (S1) are modulated by stress. Trans-synaptic cell adhesion molecules (CAMs) are implicated in stress-induced synaptic deficits. However, it remains unknown whether stress dysregulates CAMs in S1 and thereby impairs synaptic plasticity. In this study, we applied the early-life stress (ELS), chronic social defeat stress (CSDS), and chronic restraint stress paradigms and measured the mRNA levels of nectin1 in S1 of wild-type and conditional forebrain corticotropin-releasing hormone receptor 1 type (CRHR1) conditional knockout mice. We found that ELS increased nectin1 mRNA levels in S1 in adult but not adolescent mice. Moreover, CSDS increased the nectin1 mRNA levels in S1 in adult mice via the CRH-CRHR1 system. Our findings suggest that S1 is vulnerable to repeated stress exposures at some life stages, and dysregulated nectin1 expression may underlie stress-induced structural and functional abnormalities in S1.

Keywords:

stress, nectin1, primary somatosensory cortex, corticotropin-releasing hormone
Received: 30 March 2022 Revised: 30 July 2022 Accepted: 02 September 2022 Published: 22 September 2022
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Publication history

Received: 30 March 2022
Revised: 30 July 2022
Accepted: 02 September 2022
Published: 22 September 2022

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© The Author(s) 2022

Acknowledgements

We thank the Core Facilities of Zhejiang University Institute of Neuroscience for technical assistance. This work was supported by the National Natural Science Foundation of China (No. 81971260) and the Fundamental Research Funds for the Central Universities.

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