PV network plasticity mediated by neuregulin1-ErbB4 signalling controls fear extinction

被引：22

作者：

Chen, Yi-Hua ^{[1
,2
]}

Hu, Neng-Yuan ^{[1
]}

Wu, Ding-Yu ^{[1
]}

Bi, Lin-Lin ^{[1
]}

Luo, Zheng-Yi ^{[1
]}

Huang, Lang ^{[1
]}

Wu, Jian-Lin ^{[1
]}

Wang, Meng-Ling ^{[1
]}

Li, Jing-Ting ^{[1
]}

Song, Yun-Long ^{[1
]}

Zhang, Sheng-Rong ^{[1
]}

Jie, Wei ^{[1
]}

Li, Xiao-Wen ^{[1
]}

Zhang, Shi-Zhong ^{[2
]}

Yang, Jian-Ming ^{[1
]}

Gao, Tian-Ming ^{[1
]}

机构：

[1] Southern Med Univ, Guangdong Hong Kong Macao Greater Bay Area Ctr Br, Sch Basic Med Sci,Key Lab Mental Hlth,Minist Educ, Dept Neurobiol,State Key Lab Organ Failure Res, Guangzhou 510515, Peoples R China

[2] Southern Med Univ, Zhujiang Hosp, Dept Neurosurg, Guangzhou 510515, Peoples R China

来源：

MOLECULAR PSYCHIATRY | 2022年 / 27卷 / 02期

基金：

中国博士后科学基金; 中国国家自然科学基金;

关键词：

SYNAPTIC PLASTICITY; SACCHAROMYCES-CEREVISIAE; AMYGDALA INPUTS; EXPRESSION; MEMORY; PROTEIN; ERBB4; INTERNEURONS; MECHANISMS; CIRCUITS;

D O I：

10.1038/s41380-021-01355-z

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Neuroplasticity in the medial prefrontal cortex (mPFC) is essential for fear extinction, the process of which forms the basis of the general therapeutic process used to treat human fear disorders. However, the underlying molecules and local circuit elements controlling neuronal activity and concomitant induction of plasticity remain unclear. Here we show that sustained plasticity of the parvalbumin (PV) neuronal network in the infralimbic (IL) mPFC is required for fear extinction in adult male mice and identify the involvement of neuregulin 1-ErbB4 signalling in PV network plasticity-mediated fear extinction. Moreover, regulation of fear extinction by basal medial amygdala (BMA)-projecting IL neurons is dependent on PV network configuration. Together, these results uncover the local molecular circuit mechanisms underlying mPFC-mediated top-down control of fear extinction, suggesting alterative therapeutic approaches to treat fear disorders.

引用

收藏

页码：896 / 906

页数：11

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