We report that blockade of KOR elicits effects similar to ethanol on GABAergic transmission in CeA. Interestingly, norBNI occluded or prevented the effect of ethanol. This finding differs from recent results reported from CeA slice recordings in mice that showed increased facilitation of GABAergic transmission by ethanol in slices from KOR knockout mice, and in slices from wild-type mice pre-treated with norBNI (Kang-Park et al., 2013). In that study, the facilitatory effect of ethanol alone on GABAergic transmission was significantly lower (14%) than values we have reported in rats (40–50% in this study as well as Roberto et al. 2003 and 2010), suggesting a differential ethanol sensitivity and/or mechanism of action in CeA of mice and rats. In addition, KOR distribution and KOR modulation of GABAergic transmission in CeA may also differ between mice and rats, since the Kang-Park et al. (2013) study reported that approximately 50% of recorded CeA neurons did not respond to KOR antagonism (25% in our study) and 40% did not respond to KOR agonism (15% in our study).
