Evidence seems to indicate that the anxiolytic effects of centrally administered neuropeptide Y (NPY) are mediated by the central nucleus of the amygdala. Because findings seem to indicate that ethanol may be self-administered partially for its anxiolytic effects, it was hypothesized that NPY, microinjected into the central nucleus of the amygdala, would decrease ethanol intake. In this study, we examined the effects of NPY, administered into the central nucleus of the amygdala, on ethanol, sucrose, and food consumption, as well as the concomitant effects of NPY on cortical electroencephalographic activity. Wistar rats were implanted with cortical recording electrodes and cannulae above the central amygdaloid nuclei, after use of a sucrose-substitution procedure, to establish ethanol self-administration. Neuropeptide Y (0-250 pmol/0.5 micro l) was infused into the amygdala before drinking sessions, when 10% ethanol (10 E), 2% sucrose (2S), or food was available. Consumption, locomotor activity, and cortical electroencephalographic activity were then monitored concurrently. Neuropeptide Y had no effect on the intake of 10 E, 2S, or food, nor on the cortical electroencephalographic or locomotor activity. However, as reported previously, distinct changes in the electroencephalogram were associated with consumption of ethanol and sucrose. Cortical power in the 6-8 Hz frequency range was significantly increased during the beginning of the sucrose and ethanol sessions, with greater increases observed during the sucrose session. Overall, these findings support the suggestion that NPY administration into the central nucleus of the amygdala does not alter consumption of 10 E, 2S, or food, nor the cortical electroencephalographic or locomotor activity.