Studies have shown that chronic alcohol exposure alters NPY function and this may contribute to increased stress/anxiety associated with dependence as well as increased propensity to drink. Early studies indicated that NPY administration reduced elevated drinking in dependent animals (Thorsell et al., 2005a, c). More recent work has focused on NPY actions in the CeA in the context of dependence (Gilpin et al., 2015). For example, increased anxiety during withdrawal from chronic alcohol exposure was associated with decreased NPY expression in CeA (Roy and Pandey, 2002). Further, direct injection of NPY into the CeA reduced excessive alcohol consumption in dependent rats (Gilpin et al., 2008a), an effect possibly related to modulation of GABA transmission in the CeA (Gilpin et al., 2011). Recent work also points to interactions between NPY and CRF within the BNST as a site important for mediating stress influences on alcohol drinking (Pleil et al., 2015).
