Results from human postmortem studies shed some light on the effects of chronic alcohol on the OXT system. In male subjects with alcohol use disorder, OXT peptide immunoreactivity was decreased in both the SON and PVN compared to controls (Sivukhina et al., 2006). More recently, Lee et al. (2017b) reported a significant increase in Oxt mRNA in the PFC of human post-mortem AUD subjects compared to controls. In addition, the authors reported hypertrophy of OXT producing neurons in the hypothalamus in AUD patients, in concordance with previous evidence to suggesting that this effect is attributable to chronic alcohol exposure (Madeira et al., 1993). Congruent with these findings, a loss of hypothalamic OXT neurons after prolonged alcohol intake has been reported in animal studies (Silva et al., 2002, Stevenson et al., 2017b). Following repeated cycles of chronic intermittent alcohol vapor exposure to induce dependence in rats, Hansson et al. (2018) reported that Oxt mRNA levels were reduced in the NAc following acute alcohol exposure as well as during early withdrawal, but increased after prolonged (3 weeks) abstinence, suggesting dynamic dependence-related neuroadaptation
