This dissertation investigated the neural circuitry underlying baseline ethanol consumption and dependence-induced increases in alcohol intake. Focusing on the central extended amygdala (cEA), lesions were performed in the bed nucleus of the stria terminalis (BNSTLP), central nucleus of the amygdala (CeA), and nucleus accumbens (NAc) shell. Results showed these regions contribute to baseline ethanol consumption in limited access paradigms but are not required for the increased intake induced by chronic intermittent ethanol vapor exposure. c-fos analyses identified activation of the NAc shell and core during heightened ethanol consumption. Together, these findings suggest distinct neural mechanisms underlie baseline drinking and dependence-related escalation.
