Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (45)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Slawecki, C. J.
Right arrow Articles by Ehlers, C. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Slawecki, C. J.
Right arrow Articles by Ehlers, C. L.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Alcohol and Alcoholism Vol. 34, No. 3, pp. 289-299, 1999
© 1999 Medical Council on Alcoholism

EFFECTS OF CHRONIC ETHANOL EXPOSURE ON NEUROPHYSIOLOGICAL RESPONSES TO CORTICOTROPIN-RELEASING FACTOR AND NEUROPEPTIDE Y

C. J. Slawecki*, C. Somes and C. L. Ehlers

The Scripps Research Institute, Department of Neuropharmacology, CVN-14, 10550 North Torrey Pines Road, La Jolla, CA 902037, USA

Received 3 August 1998; first review notified 2 November 1998; accepted 26 November 1998

Stress has been reported to influence ethanol consumption and relapse in abstinent alcoholics. The present study examined if prolonged alterations in neurophysiological responses to corticotropin-releasing factor (CRF) and neuropeptide Y (NPY), peptides known to influence stress responses, would persist during protracted ethanol abstinence. Male Wistar rats were chronically exposed to ethanol vapour (EtOH group) or air (control group) for 6 weeks. Upon removal from the vapour chambers, recording electrodes were implanted in the cortex and amygdala. The effects of intracerebroventricular infusions of CRF and NPY on electroencephalogram (EEG) and event-related potentials (ERPs) were then assessed 10–15 weeks after withdrawal from ethanol. Following 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 frontal 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 NPY. CRF significantly increased cortical power (6–8 Hz) and increased cortical EEG stability in the EtOH group, compared to controls. Additionally, NPY significantly decreased the amplitude of the N1 ERP component in the amygdala of the EtOH group, but not in the control group. This enhanced sensitivity to CRF and NPY following chronic ethanol exposure and abstinence suggests that these peptidergic systems may play a role in the symptomatology of the prolonged abstinence syndrome.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 J. Neurosci.Home page
W. Francesconi, F. Berton, V. Repunte-Canonigo, K. Hagihara, D. Thurbon, D. Lekic, S. E. Specio, T. N. Greenwell, S. A. Chen, K. C. Rice, et al.
Protracted Withdrawal from Alcohol and Drugs of Abuse Impairs Long-Term Potentiation of Intrinsic Excitability in the Juxtacapsular Bed Nucleus of the Stria Terminalis
J. Neurosci., April 29, 2009; 29(17): 5389 - 5401.
[Abstract] [Full Text] [PDF]

Home page
 Pharmacol. Rev.Home page
Z. Sarnyai, Y. Shaham, and S. C. Heinrichs
The Role of Corticotropin-Releasing Factor in Drug Addiction
Pharmacol. Rev., June 1, 2001; 53(2): 209 - 244.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.