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A critical role is elucidated for the VMHCaMKIIα-LHGABA circuit in mediating stress-induced reinstatement of Alp-CPP in male mice, thereby advancing the understanding of the neural mechanisms underlying Alp reinstatement and providing novel insights for the prevention and treatment of BZD addiction.
Results reveal a previously unidentified role for Bmal1 deficiency in the PrL in driving SCZ-relevant negative symptoms and cognitive dysfunction, and provide experimental evidence supporting a putative role for dysregulated circadian clock gene expression in the pathogenesis of SCZ.
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