Cacna1c in the Prefrontal Cortex Regulates Depression-Related Behaviors via REDD1.

ABSTRACT: The CACNA1C gene that encodes the L-type Ca²⁺ channel (LTCC) Ca_v1.2 subunit has emerged as a candidate risk gene for multiple neuropsychiatric disorders including bipolar disorder, major depressive disorder, and schizophrenia, all marked with depression-related symptoms. Although cacna1c heterozygous (HET) mice have been previously reported to exhibit an antidepressant-like phenotype, the molecular and circuit-level dysfunction remains unknown. Here we report that viral vector-mediated deletion of cacna1c in the adult prefrontal cortex (PFC) of mice recapitulates the antidepressant-like effect observed in cacna1c HET mice using the sucrose preference test (SPT), forced swim test (FST), and tail suspension test (TST). Molecular studies identified lower levels of REDD1,

SUBMITTER: Kabir ZD 

PROVIDER: S-EPMC5561335 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature