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• W4386795933 abstract "Major depressive disorder is a severe psychiatric disorder that afflicts ~17% of the world population. Neuroimaging investigations of depressed patients have consistently reported the dysfunction of the basolateral amygdala in the pathophysiology of depression. However, how the BLA and related circuits are implicated in the pathogenesis of depression is poorly understood.Here, we combined fiber photometry, immediate early gene expression (c-fos), optogenetics, chemogenetics, behavioral analysis, and viral tracing techniques to provide multiple lines of evidence of how the BLA neurons mediate depressive-like behavior.We demonstrated that the aversive stimuli elevated the neuronal activity of the excitatory BLA neurons (BLACAMKII neurons). Optogenetic activation of CAMKII neurons facilitates the induction of depressive-like behavior while inhibition of these neurons alleviates the depressive-like behavior. Next, we found that the chemogenetic inhibition of GABAergic neurons in the BLA (BLAGABA ) increased the firing frequency of CAMKII neurons and mediates the depressive-like phenotypes. Finally, through fiber photometry recording and chemogenetic manipulation, we proved that the activation of BLAGABA neurons inhibits BLACAMKII neuronal activity and alleviates depressive-like behavior in the mice.Thus, through evaluating BLAGABA and BLACAMKII neurons by distinct interaction, the BLA regulates depressive-like behavior." @default.
• W4386795933 created "2023-09-17" @default.
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• W4386795933 date "2023-09-16" @default.
• W4386795933 modified "2023-09-26" @default.
• W4386795933 title "Potentiated <scp>GABAergic</scp> neuronal activities in the basolateral amygdala alleviate stress‐induced depressive behaviors" @default.
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• W4386795933 doi "https://doi.org/10.1111/cns.14422" @default.
• W4386795933 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37715582" @default.
• W4386795933 hasPublicationYear "2023" @default.
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