Cj. Slawecki et al., Effects of chronic ethanol exposure on neurophysiological responses to corticotropin-releasing factor and neuropeptide Y, ALC ALCOHOL, 34(3), 1999, pp. 289-299
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.