Many in vivo studies point to the involvement of NPY in mediating some of the behavioral effects of EtOH (Caberlotto et al. 2001; Cippitelli et al. 2010; Rimondini et al. 2005). NPY KO mice show increased EtOH preference but blunted behavioral responses to EtOH, while NPY overexpressors show a lower preference and increased sensitivity to EtOH (Thiele et al. 1998). Likewise, increased NPY expression in the CeA was noted in two independent strains of alcohol-preferring rats (Hwang et al. 1999). There were increased levels of NPY in the paraventricular nucleus of the hypothalamus (PVN) and arcuate nucleus of EtOH-preferring rats and decreased NPY levels in the CeA of EtOH-preferring rats, suggesting an inverse relationship between NPY levels in the CeA and EtOH consumption. Additionally, alcohol-preferring rats show significant decreases in both cAMP-responsive element-binding protein (CREB) and NPY levels in the CeA and medial amygdala, but not the basolateral amygdala (Pandey et al. 2005). Further, virally mediated alterations in NPY levels in the CeA differentially affect EtOH consumption in rats with low and high basal levels of anxiety (Primeaux et al.
