Electrophysiologic findings suggest that NPY and EtOH have a similar profile of actions (Ehlers et al. 1998a, b, 1999). Increased sensitivity to NPY and CRF was observed in cortex and amygdala after chronic EtOH exposure, as measured by EEG activity and event-related potentials (Slawecki et al. 1999). Modulation of amygdala EEGs by NPY differs in naïve P and NP rats, suggesting that NPY has different neuromodulatory effects in these two strains (Ehlers et al. 1998a). Furthermore, NPY antagonizes the effects of CRF in the amygdala. However, to date neither the cellular actions of NPY in neither the CeA nor its interactions with EtOH or CRF, have been fully characterized. Recent findings by Gilpin et al. (2009, 2011) show that NPY superfusion decreased baseline GABAergic transmission in CeA slices and blocked the alcohol-induced enhancement of inhibitory transmission in CeA via presynaptic Y2 receptors.
