Effects of chronic ethanol exposure on neurophysiological responses to corticotropin-releasing factor and neuropeptide Y

Stress has been reported to influence ethanol consumption and relapse in ab stinent alcoholics. The present study examined if prolonged alterations in neurophysiological responses to corticotropin-releasing factor (CRF) and ne uropeptide Y (NPY), peptides known to influence stress responses, would per sist during protracted ethanol abstinence, Male Wistar rats were chronicall y exposed to ethanol vapour (EtOH group) or air (control group) for 6 weeks . Upon removal from the vapour chambers, recording electrodes were implante d in the cortex and amygdala. The effects of intracerebroventricular infusi ons of CRF and NPY on electroencephalogram (EEG) and event-related potentia ls (ERPs) were then assessed 10-15 weeks after withdrawal from ethanol. Fol lowing abstinence from ethanol, the EtOH group displayed increased power in the 6-8 Hz Frequency range and increased stability in the cortical EEG. In addition, in the EtOH group the amplitude of the P2 ERP component in the f rontal cortex was decreased and the latency of the P3 ERP component in the parietal cortex was delayed, compared to the control group during baseline recording conditions. The EtOH group was also more responsive to CRF and NP Y. CRF significantly increased cortical power (6-8 Hz) and increased cortic al EEG stability in the EtOH group, compared to controls. Additionally, NPY significantly decreased the amplitude of the N1 ERP component in the amygd ala of the EtOH group, but not in the control group. This enhanced sensitiv ity to CRF and NPY following chronic ethanol exposure and abstinence sugges ts that these peptidergic systems may play a role in the symptomatology of the prolonged abstinence syndrome.