GABAA receptor antagonism in the extended amygdala decreases ethanol self-administration in rats.

The present experiments examined the role of the extended amygdala GABAA receptors in the regulation of ethanol consumption in rats. The areas of the extended amygdala studied included the central nucleus of the amygdala, the bed nucleus of the stria terminalis, and the shell of the nucleus accumbens. The effects of bilateral microinjections of a competitive GABAA receptor antagonist, 2-(3-carboxypropyl)-3-amino-6-(4-methoxyphenyl)pyridazinium bromide (SR 95531), on ethanol consumption were assessed in Wistar rats that were trained to respond for oral ethanol (10% w/v) in a two-lever, free-choice operant task during 30-min sessions using a saccharin fading procedure. Injections of SR 95531 into the central amygdaloid nucleus decreased ethanol responding significantly at doses of 2 and 4 ng without affecting water responding. SR 95531 injections into the bed nucleus of the stria terminalis reduced ethanol responding significantly at the 8 ng and 16 ng dose, while only the 16 ng dose produced a significant effect in the shell of the nucleus accumbens. Cumulative response patterns showed that intra-amygdaloid injections did not disrupt the initiation of responding. Injections into the bed nucleus of the stria terminalis and the nucleus accumbens, however, suppressed both ethanol and water responding at the highest SR 95531 doses during the first minutes. These findings suggest that GABAA receptors in the extended amygdala may be involved in the mediation of some aspects of ethanol reward.