the prodynorphin-deficient mice did not exhibit stress-enhanced drinking observed in wildtype mice (Sperling et al., 2010). In another study, prodynorphin-deficient male and female mice consumed more ethanol compared to their wildtype littermates in a home-cage free-choice drinking paradigm, but the null mutant mice did not exhibit a transient increase in drinking following footshock stress that was observed in the wildtype mice (Racz et al., 2013). Thus, the ability of stress to elevate ethanol consumption is lost when dynorphin is genetically deleted or KORs are pharmacologically blocked. Collectively, these results suggest that the DYN/KOR system plays a role in contributing to stress-induced elevation in ethanol consumption.
