ATP release from the amygdala-prefrontal pathway regulates vulnerability to social stress in male mice - PubMed
5 hours ago
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- #depression
- ATP deficiency in the medial prefrontal cortex (mPFC) is linked to major depressive disorder under stress.
- Stress-susceptible mice show reduced basal and reward-evoked ATP release in mPFC, reversible by fluoxetine.
- Slc17a9 (VNUT) is downregulated in mPFC of stress-susceptible mice; its knockout in neurons induces depressive-like behaviors.
- Knocking down Slc17a9 in basolateral amygdala (BLA)-mPFC neurons reproduces ATP deficits and depression-like symptoms.
- Microinjection of nonhydrolyzable ATP analogs (ATPγS) into mPFC reverses these behavioral deficits.
- The BLA-mPFC pathway bidirectionally regulates depressive behaviors via ATP release, highlighting a circuit-specific mechanism.
- Study emphasizes stress-induced ATP deficiency as key in depression pathogenesis and stress vulnerability.