Optogenetic inactivation of CRF neurons in the central nucleus of the amygdala decreases escalation of alcohol consumption and intensity of withdrawal in rodent models of alcoholism. The findings suggest a potential target for treating excessive drinking in alcohol use disorder.
Specific neurons in the central nucleus of the amygdala regulate alcohol consumption.
Administering oxytocin blocks the enhanced motivation for drinking alcohol that fuels alcohol use disorder by blocking GABA signaling in the central nucleus of the amygdala.
Teenage binge drinking is linked to altered gene expression in the brain, specifically the central nucleus of the amygdala. Adolescent rats exposed to alcohol had increased levels of miR-137, resulting in lower expression of proteins essential for healthy neuron growth. During adulthood, these rats displayed higher levels of anxiety and an increased preference for alcohol consumption.