Supported in part by the Washington State University Alcohol and Drug Abuse Program and by NIH Grants NS25378, NS27250, and RO1AA13248.
Diurnal Effects of Acute and Chronic Administration of Ethanol on Sleep in Rats
Version of Record online: 11 APR 2006
Alcoholism: Clinical and Experimental Research
Volume 26, Issue 8, pages 1153–1161, August 2002
How to Cite
Kubota, T., De, A., Brown, R. A., Simasko, S. M. and Krueger, J. M. (2002), Diurnal Effects of Acute and Chronic Administration of Ethanol on Sleep in Rats. Alcoholism: Clinical and Experimental Research, 26: 1153–1161. doi: 10.1111/j.1530-0277.2002.tb02651.x
- Issue online: 11 APR 2006
- Version of Record online: 11 APR 2006
- Received for publication December 24, 2001; accepted April 25, 2002.
- REM Sleep;
- Spectral Analysis
Background Disturbances in sleep patterns are a complicating factor in recovery from alcoholism. The effects of acute and chronic alcohol treatments on sleep in rats were determined.
Methods Adult male Sprague-Dawley rats were acclimated to a temperature-controlled chamber, and electromyograms and electroencephalograms (EEGs) were obtained during 23-hr recording sessions. Time spent in rapid eye movement sleep (REMS) and non-REM sleep (NREMS), EEG slow-wave activity (SWA) during NREMS, a spectral analysis of the EEG by fast Fourier transform, and brain temperatures were determined.
Results Acute exposure to alcohol (2.3 and 3.0 g/kg) by gastric intubation at the beginning of dark onset produced an increase in NREMS and a suppression of SWA. Spectral analysis revealed that during the first 4 hr there was a small increase in very-low-frequency bands (0.5–2 Hz), with a suppression of higher-frequency bands. This was followed by a suppression of low-frequency bands. A dose of 3.0 g/kg at light onset caused an increase in NREMS and a suppression of SWA. Spectral analysis revealed a suppression of low-frequency bands throughout the first 12 hr of recording but no change on high-frequency bands with light-onset alcohol. Chronic treatment with alcohol (6% alcohol in a liquid diet with pair-fed isocaloric controls) for 3 weeks produced an increase in NREMS and a decrease in EEG power density in frequency bands above 2 Hz. Chronic alcohol also reduced the circadian variation of REMS, an effect that showed a rebound 1 week after the alcohol treatment was terminated. Two weeks after the alcohol treatment was stopped, NREMS and REMS values returned to baseline.
Conclusions These results demonstrate differences in the effect of acute alcohol on sleep depending on the time of administration and demonstrate that distinct alterations in sleep patterns are induced by chronic treatments in as little as 3 weeks.