Although limited in scope, several studies have examined mechanisms that underlie DYN/KOR modulation of behavioral effects of ethanol. These studies have primarily focused on DYN/KOR adaptations in the nucleus accumbens and central nucleus of the amygdala. A number of studies have provided evidence that the DYN/KOR system exerts effects on the motivational effects of ethanol (and other drugs of abuse) in part by modulating mesolimbic dopamine (DA) release. Within the nucleus accumbens, KORs are located on DA terminals and inhibit DA release when activated (Svingos, 2011). Acute ethanol administration (via ip injection) increases DA release in the nucleus accumbens, and this effect is enhanced in KOR knockout mice or following pretreatment with a KOR antagonist (nor-BNI) in C57BL/6J mice (Zapata and Shippenberg, 2006). However, during operant ethanol self-administration, ethanol-induced DA release in the nucleus accumbens was blocked by nor-BNI, although a delayed DA increase was observed at the end of the ethanol access period (Doyon et al., 2006). Conversely, KOR activation has been shown to attenuate ethanol-induced DA release in the nucleus accumbens (Lindholm et al., 2007). The same report
