Circadian variations in vigilance states in the alcohol-dependent rat

Rouhani, S.; Emmanouilidis, E.; Tran, Giang N.; Durlach, J; Payan, Christine; Fermanian, Jean‐David; Manicom, R; Soulairac, A; Poenaru, S

doi:10.1016/0031-9384(90)90203-g

Cited by 11 publications

(9 citation statements)

References 12 publications

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“…Consistent with clinical reports, studies of sleep in the rat report reduced sleep time during alcohol withdrawal after chronic exposure (Ehlers and Slawecki, 2000; Gillin et al, 1990; Kubota et al, 2002; Mendelson et al, 1978; Rouhani et al, 1998, 1990). The impact of ethanol (EtOH) on sleep architecture in animal models is less consistent, with REM sleep reported to increase (Mendelson et al, 1978), decrease (Rouhani, et al, 1990), or undergo circadian variation (Kubota et al, 2002) during withdrawal. Similarly, studies have shown non‐REM sleep to increase (Kubota et al, 2002; Rouhani et al, 1998, 1990) or remain unchanged (Ehlers and Slawecki, 2000).…”

supporting

confidence: 68%

Disruptions in Sleep Time and Sleep Architecture in a Mouse Model of Repeated Ethanol Withdrawal

Veatch¹

2006

Alcoholism Clin & Exp Res

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supporting

confidence: 68%

Disruptions in Sleep Time and Sleep Architecture in a Mouse Model of Repeated Ethanol Withdrawal

Veatch¹

2006

Alcoholism Clin & Exp Res

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“…This would suggest that perhaps REMS is more sensitive to the amount of alcohol (observed in both studies when 6% in liquid diet was used for either 3 weeks or 6 weeks) but that changes in SWS require longer treatments (decreased SWS in the light period was only observed after 6 weeks of 6% alcohol in liquid diet). In further agreement that REMS is more sensitive to the amount of alcohol given, Rouhani et al (1990) reported a decrease of REMS in the light period after 2 weeks when alcohol (10 g/kg/day) was given by gastric infusion. This is an exposure level very similar to our 6% in liquid diet.…”

Section: Discussionmentioning

confidence: 60%

“…Two prior studies have focused specifically on the alcohol induced pathologies that follow chronic alcohol exposure for 2-3 weeks. In the study by Rouhani et al (1990) alcohol was given by scheduled infusions via an indwelling gastric catheter. After 13 days they observed decreases in percent SWS and REMS and increase in wake only in the light period.…”

Section: Introductionmentioning

confidence: 99%

Dose–response study of chronic alcohol induced changes in sleep patterns in rats

2008

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The goal of the present study was to determine an optimum exposure regimen for alterations in sleep induced by chronic alcohol treatments in rats. We used two different exposure routes (alcohol in water and alcohol in liquid diet at two different doses in each regimen (6% and 12% alcohol in water and 3% and 6% alcohol in liquid diet)). All treatments were for 6 weeks. We found the effects of the 6% and 12% in water and 3% in liquid diet to be very similar; all three produced increases in slowwave sleep (SWS) only in the dark period with no changes in rapid-eye-movement sleep (REMS). On the other hand 6% alcohol in liquid diet caused much more dramatic changes, with alterations in both SWS and REMS in both the dark and light periods. These animals spent less time in SWS and REMS during the light period but more time in SWS and REMS in the dark period. Additionally, the variation of slow-wave amplitude (SWA) across day and night in this group of alcoholic animals is blunted with the loss of the peak of SWA at the beginning of light onset compared to the other groups. We conclude that future alcohol treatment regimens used to investigate the effects of alcohol on sleep in adult rats should use an exposure protocol of at least 6 weeks with 6% alcohol in liquid diet.

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“…Disruptions in sleep and circadian rhythms can persist through extended periods of abstinence, and persisting chronobiological disruptions may in turn promote relapse to drinking (Brower, 2003;Drummond et al, 1998;Gillin et al, 1994;Kuhlwein et al, 2003;Landolt and Gillin, 2001). These effects are probably a direct consequence of chronic excessive ethanol intake, since similar alterations in sleep and circadian rhythms (Ehlers and Slawecki, 2000;El-Mas and Abdel-Rahman, 2000;Kakihana and Moore, 1976;Rajakrishnan et al, 1999;Rouhani et al, 1990) and in mood regulation (Kliethermes et al, 2002;Overstreet et al, 2002) occur in experimental animals during chronic ethanol treatment and/or ethanol withdrawal.…”

Section: Circadian Rhythms and Cellular Clocksmentioning

confidence: 99%

Alcohol Consumption and the Body???s Biological Clock

Spanagel¹,

Rosenwasser²,

Schumann³

et al. 2005

Alcoholism: Clinical & Experimental Research

154

122

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This review summarizes new findings on the bidirectional interactions between alcohol and the clock genes, underlying the generation of circadian rhythmicity. At the behavioral level, both adult and perinatal ethanol treatments after the free-running period and light response of the circadian clock in rodents; genetic ethanol preference in alcohol-preferring rat lines is also associated with alterations in circadian pacemaker function. At the neuronal level, it has been shown that ethanol consumption alters the circadian expression patterns of period (per) genes in various brain regions, including the suprachiasmatic nucleus. Notably, circadian functions of beta-endorphin-containing neurons that participate in the control of alcohol reinforcement become disturbed after chronic alcohol intake. In turn, per2 gene activity regulates alcohol intake through its effects on the glutamatergic system through glutamate reuptake mechanisms and thereby may affect a variety of physiological processes that are governed by our internal clock. In summary, a new pathologic chain has been identified that contributes to the negative health consequences of chronic alcohol intake. Thus, chronic alcohol intake alters the expression of per genes, and as a consequence, a variety of neurochemical and neuroendocrine functions become disturbed. Further steps in this pathologic chain are alterations in physiological and immune functions that are under circadian control, and, as a final consequence, addictive behavior might be triggered or sustained by this cascade.

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Circadian variations in vigilance states in the alcohol-dependent rat

Cited by 11 publications

References 12 publications

Disruptions in Sleep Time and Sleep Architecture in a Mouse Model of Repeated Ethanol Withdrawal

Disruptions in Sleep Time and Sleep Architecture in a Mouse Model of Repeated Ethanol Withdrawal

Dose–response study of chronic alcohol induced changes in sleep patterns in rats

Alcohol Consumption and the Body???s Biological Clock

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