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Effect of Gabapentin on Sleep and Event‐Related Oscillations (EROs) in Rats Exposed to Chronic Intermittent Ethanol Vapor and Protracted Withdrawal
Author(s) -
SanchezAlavez Manuel,
Wills Derek N.,
Amodeo Leslie,
Ehlers Cindy L.
Publication year - 2018
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/acer.13588
Subject(s) - gabapentin , anesthesia , ethanol , medicine , chemistry , alternative medicine , organic chemistry , pathology
Background Disturbances in sleep architecture, especially reductions in slow‐wave sleep (SWS), are symptoms commonly observed in individuals with alcohol use disorders. Recent clinical trials have demonstrated that the anticonvulsant and analgesic drug gabapentin may have therapeutic value in normalizing sleep quality in recovering alcoholics. However, the brain mechanisms underlying this improvement in sleep following gabapentin treatment remain unknown. Methods In this study, adult Wistar rats were exposed to 8 weeks of chronic intermittent ethanol [EtOH] vapor (blood EtOH concentrations averaged 128.2 ± 17.4 mg/dl) or control conditions and then withdrawn. Sleep electroencephalograms [EEGs] and event‐related oscillations (EROs) were evaluated at baseline prior to EtOH exposure and 24 hours following EtOH withdrawal. Four weeks following EtOH withdrawal the effects of saline and 2 doses of gabapentin (30, 120 mg/kg), on EROs and sleep EEGs, were evaluated. Results As compared to baseline, 24 hours following alcohol withdrawal SWS became fragmented as indexed by a significant increase in the number and a decrease in the duration of SWS episodes. Compared to controls, the EtOH‐exposed group had more ERO energy in the beta frequency band in the parietal cortex. Gabapentin induced a dose‐dependent decrease in the latency to the first SWS episode, and a reduction in sleep fragmentation. Gabapentin also produced a dose‐dependent increase in ERO energy in the control group that was significantly attenuated in the EtOH‐exposed group in the theta, and beta frequency bands. Conclusions Taken together, these studies suggest that gabapentin can reverse some of the alcohol‐induced sleep and EEG deficits but does not eliminate all of the enduring brain effects of EtOH exposure.