Corticosterone antagonist or TrkB agonist attenuates schizophrenia-like behavior in a mouse model combining Bdnf-e6 deficiency and developmental stress.

ABSTRACT: While schizophrenia pathogenesis involves both genetic and environmental factors, their specific combinations remain ill-defined. Here we show that deficiency in promoter VI-driven BDNF expression, combined with early-life adversity, results in schizophrenia-like endo-phenotypes. Promoter VI mutant mice (Bdnf-e6 ^-/- ), when exposed to postnatal stress including hypoxia or social isolation, exhibited deficits in social interactions, spatial memory, and sensorimotor gating reflected by prepulse inhibition (PPI). Neither early-life stress nor Bdnf-e6 deficiency alone caused these abnormalities. Moreover, postnatal stress increased blood corticosterone levels of wild-type mice, and administration of corticosterone to Bdnf-e6^-/- mice without ear

SUBMITTER: Chen Y 

PROVIDER: S-EPMC9250029 | biostudies-literature | 2022 Jul

REPOSITORIES: biostudies-literature