Electrophysiological response to neuropeptide Y (NPY): in alcohol-naive preferring and non-preferring rats.

Electroencephalograms (EEGs) and event-related potentials (ERPs) to auditory stimuli were recorded following intracerebroventricular administration of neuropeptide Y (saline, NPY: 1.0, 3.0 nmol) in two lines of rats that have been genetically selected for alcohol preferring (P) or non-preferring (NP) behaviors. Previous studies have demonstrated that NPY has a distinct electrophysiological profile that is similar to that of ethanol. In outbred Wistar rats, both NPY and ethanol produced highly significant decreases in the amplitude and increases in the latency of the N1 component of the ERP to all three auditory stimuli. Because the N1 has been associated with attention, these data suggest that both NPY and alcohol may diminish attentional processes. In the present study, NPY-induced decreases in N1 amplitude were also found, but only to the frequently presented tone. This suggests that both P and NP rats may have attenuated responses to NPY's effects on attention/arousal. Like outbred Wistars, P and NP rats were also found to have significant NPY-induced increases in N1 latency in the cortex and hippocampus. However, in the amygdala, while P rats evidenced increases in N1 latency and decreases in N1 amplitudes, NP rats displayed the opposite effects. Spectral analysis revealed that NPY also produced differential EEG responses in P and NP rats. In previous studies in outbred Wistar rats NPY has been found to produce slowing of delta (1-2 Hz) frequencies at the 1-nmol dose and reductions in power, particularly in the higher frequencies in the amygdala, at the 3-nmol dose. This electrophysiological profile is not unlike what is seen following alcohol and benzodiazepines and is associated with anxiolysis. P rats were found to have this general pattern of EEG responses to NPY but attenuated suggesting that they may have reduced responses to electrophysiological measures of the anxiolytic effects of NPY. In contrast, NP rats had NPY-induced EEG effects in amygdala and frontal cortex that were opposite to those seen in P rats. These opposing responses to NPY tended to produce a "normalization" of the power differences that existed between the two rat lines at baseline. Taken together with previous findings that P rats have decreased NPY concentrations in limbic and frontal cortical sites, these data suggest that differences in the regulation of NPY neurons may contribute to the expression of behavioral preference for ethanol consumption in these rat lines.