Ventral Hippocampal CA1 GADD45B Regulates Susceptibility to Social Stress by Influencing NMDA Receptor‑Mediated Synaptic Plasticity  

作　　者：Mengbing Huang Jian Bao Xiaoqing Tao Yifan Niu Kaiwei Li Ji Wang Xiaokang Gong Rong Yang Yuran Gui Hongyan Zhou Yiyuan Xia Youhua Yang Binlian Sun Wei Liu Xiji Shu 

机构地区：[1]Hubei Key Laboratory of Cognitive and Affective Disorders,Institutes of Biomedical Sciences,School of Medicine,Jianghan University,Wuhan 430056,China

出　　处：《Neuroscience Bulletin》2025年第3期406-420,共15页神经科学通报(英文版)

基　　金：supported by the National Natural Science Foundation of China(82201667,82371195,and 82304474);the Research Fund of Jianghan University(2023JCYJ15).

摘　　要：Growth arrest DNA damage-inducible protein 45β(GADD45B)has been reported to be a regulatory factor for active DNA demethylation and is implicated in the modulation of synaptic plasticity and chronic stress-related psychopathological processes.However,its precise role and mechanism of action in stress susceptibility remain elusive.In this study,we found a significant reduction in GADD45B expression specifically in the ventral,but not the dorsal hippocampal CA1(dCA1)of stress-susceptible mice.Furthermore,we demonstrated that GADD45B negatively regulates susceptibility to social stress and NMDA receptor-dependent long-term potentiation(LTP)in the ventral hippocampal CA1(vCA1).Importantly,through pharmacological inhibition using the NMDA receptor antagonist MK801,we provided further evidence supporting the hypothesis that GADD45B potentially modulates susceptibility to social stress by influencing NMDA receptor-mediated LTP.Collectively,these results suggested that modulation of NMDA receptor-mediated synaptic plasticity is a pivotal mechanism underlying the regulation of susceptibility to social stress by GADD45B.

关 键 词：Chronic stress Ventral hippocampal CA1 GADD45B NMDA receptor Synaptic plasticity 

分 类 号：R749.4[医药卫生—神经病学与精神病学]