Central nucleus of the amygdala and the effects of alcohol and alcohol-drinking behavior in rodents.

This article will review key literature on the effects of alcohol on the amygdala and the involvement of the amygdala in regulating alcohol drinking in mice and rats. Special emphasis will be placed on the central nucleus of the amygdala (CeA) because this nucleus is a major component of the extended amygdala, which has been implicated in regulating alcohol-drinking behavior. Immunocytochemical and in situ hybridization studies indicate that acute high-dose ethanol administration increases c-fos expression in GABAergic neurons within the CeA of the rat, suggesting activation of these neurons by ethanol. A similar high-dose (4 g/kg ethanol) effect on c-fos expression in the CeA of C57 mice was also observed, whereas the DBA mice showed increased c-fos expression in the CeA in the dose range of 1.25-4.0 g/kg. Studies with DBA x C57 F2 intercross mice suggest that there may be a relationship between the neuronal activating effects of ethanol in the CeA and the locomotor stimulating effects of ethanol. Studies with rats examining the effects of acute ethanol or chronic alcohol drinking on local cerebral glucose utilization (LCGU) rates (as a measure of synaptic activity) indicated that (a) acute ethanol (0.25-2.0 g/kg) had little effect on LCGU rates in the CeA; (b) basal LCGU rates were reduced in the CeA as a result of chronic alcohol drinking; and (c) oral self-administration of ethanol increased LCGU values within the CeA. Microdialysis studies demonstrated that acute ethanol (2 g/kg) injection increased dopamine (DA) and serotonin (5-HT) release in the CeA. Microinjection studies indicate that GABA(A) receptors within the CeA are involved in oral ethanol self-administration. Overall, the findings from the various studies support a role for the CeA in mediating the stimulating actions of alcohol in mice and regulating alcohol-drinking behavior in mice and rats.