A few studies have examined the effects of ethanol on DYN/KOR function in the central nucleus of the amygdala. For example, electrophysiological studies showed that pharmacological manipulation of KORs altered acute ethanol-induced increases in GABA transmission (Kang-Park et al., 2013; Gilpin et al., 2014). Further, null mutant KOR mice showed greater ethanol-induced increases in GABA-mediated synaptic inhibition (Kang-Park et al., 2013). As previously described, adaptations indicative of greater KOR signaling and dynorphin peptide expression have been also observed during withdrawal from chronic ethanol vapor exposure (Kissler et al., 2014). These reported adaptations in the central nucleus of the amygdala are thought to mediate escalated drinking and behavioral measures of dysphoria/negative affect associated with ethanol dependence and withdrawal (Kissler et al.; 2014; Kissler and Walker, 2016).
