FMRP regulates an ethanol-dependent shift in GABA_BR function and expression with rapid antidepressant properties.

ABSTRACT: Alcohol promotes lasting neuroadaptive changes that may provide relief from depressive symptoms, often referred to as the self-medication hypothesis. However, the molecular/synaptic pathways that are shared by alcohol and antidepressants are unknown. In the current study, acute exposure to ethanol produced lasting antidepressant and anxiolytic behaviours. To understand the functional basis of these behaviours, we examined a molecular pathway that is activated by rapid antidepressants. Ethanol, like rapid antidepressants, alters γ-aminobutyric acid type B receptor (GABA_BR) expression and signalling, to increase dendritic calcium. Furthermore, new GABA_BRs are synthesized in response to ethanol treatment, requiring fragile-X mental retardation protein (FMRP). Ethanol-dep

SUBMITTER: Wolfe SA 

PROVIDER: S-EPMC5052688 | biostudies-literature | 2016 Sep

REPOSITORIES: biostudies-literature