ES impairs temporal order memory, spatial working memory, novel object recognition, and spatial object recognition in adolescent male mice. ES reduces mPFC PVI density without affecting SST-INs. ES lowers mPFC PVI activity measured by c-fos and evoked action potentials. ES decreases excitatory inputs from PNs to PVIs, raising paired-pulse ratio. ES suppresses mPFC PN activity via c-fos and evoked potentials. Chemogenetic PVI inhibition mimics ES cognitive deficits. Optogenetic PVI inhibition impairs temporal order and spatial working memory. Chemogenetic PVI activation reverses ES cognitive deficits. Chemogenetic PN activation reverses ES cognitive deficits via PVIs. PN inhibition mimics ES deficits – PVI activation does not rescue when PNs inhibited. ES upregulates CRHR1 in PNs, causing PN downregulation and PVI reduction. CRHR1 knockout prevents ES-induced PVI activity drop and cognitive deficits. CRH overexpression in PNs reduces PVI activity and impairs cognition. Antalarmin restores PVI activity and reverses ES cognitive deficits. Environmental enrichment restores PVI activity and reverses ES cognitive deficits.