Identification of a prefrontal cortex-to-amygdala pathway for chronic stress-induced anxiety

Dysregulated prefrontal control over amygdala is engaged in the pathogenesis of psychiatric diseases including depression and anxiety disorders. Here we show that, in a rodent anxiety model induced by chronic restraint stress (CRS), the dysregulation occurs in basolateral amygdala projection neurons...

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Vydáno v:	Nature communications Ročník 11; číslo 1; s. 2221 - 15
Hlavní autoři:	Liu, Wei-Zhu, Zhang, Wen-Hua, Zheng, Zhi-Heng, Zou, Jia-Xin, Liu, Xiao-Xuan, Huang, Shou-He, You, Wen-Jie, He, Ye, Zhang, Jun-Yu, Wang, Xiao-Dong, Pan, Bing-Xing
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	London Nature Publishing Group UK 06.05.2020 Nature Publishing Group Nature Portfolio
Témata:	13/51 14/19 14/34 631/378 631/443 64/60 9/74 Amygdala Amygdala - physiology Animals Anxiety Anxiety - metabolism Anxiety - physiopathology Anxiety disorders Basolateral Nuclear Complex - physiology Corticosterone - pharmacology Disorders Etiology Glutamic Acid - metabolism Humanities and Social Sciences Male Mental disorders Mice Mice, Inbred C57BL multidisciplinary Neural Pathways - physiology Neurons Neurons - metabolism Optogenetics Pathogenesis Prefrontal cortex Prefrontal Cortex - physiology Restraint, Physical Science Science (multidisciplinary) Stress Stress, Psychological
ISSN:	2041-1723, 2041-1723
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Shrnutí:	Dysregulated prefrontal control over amygdala is engaged in the pathogenesis of psychiatric diseases including depression and anxiety disorders. Here we show that, in a rodent anxiety model induced by chronic restraint stress (CRS), the dysregulation occurs in basolateral amygdala projection neurons receiving mono-directional inputs from dorsomedial prefrontal cortex (dmPFC→BLA PNs) rather than those reciprocally connected with dmPFC (dmPFC↔BLA PNs). Specifically, CRS shifts the dmPFC-driven excitatory-inhibitory balance towards excitation in the former, but not latter population. Such specificity is preferential to connections made by dmPFC, caused by enhanced presynaptic glutamate release, and highly correlated with the increased anxiety-like behavior in stressed mice. Importantly, low-frequency optogenetic stimulation of dmPFC afferents in BLA normalizes the enhanced prefrontal glutamate release onto dmPFC→BLA PNs and lastingly attenuates CRS-induced increase of anxiety-like behavior. Our findings thus reveal a target cell-based dysregulation of mPFC-to-amygdala transmission for stress-induced anxiety. Dysregulated prefrontal control over amygdala has been implicated in the etiology of stress-related psychiatric disorders. Here, the authors show that the dysregulation preferentially occurs in amygdala neurons that are mono- but not bi-directionally connected with dorsomedial prefrontal cortex.
Bibliografie:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23
ISSN:	2041-1723 2041-1723
DOI:	10.1038/s41467-020-15920-7