REM-sleep deprivation-induced increase in ethanol intake: Role of brain monoaminergic neurons
Abstract
The ethanol intake of Long-Evans male rats was recorded before, during and after deprivation of rapid eye movement (REM) sleep produced with the flowerpot technique modified by using a cuff pedestal and electrified grid floor instead of water. Ethanol intake increased significantly during REM-sleep deprivation. A rebound decrease in ethanol drinking was then observed during the REM-rebound phase immediately after the termination of REM-sleep deprivation. Because REM-sleep deprivation has been reported to impair the function of central monoamine neuronal systems and because some studies have implicated these systems in the control of voluntary ethanol intake, we studied whether different monoamine uptake blocking agents could antagonize the increase in ethanol intake caused by REM-sleep deprivation. After three days of REM-sleep deprivation, the rats were given uptake blocking agents for serotonin (citalopram, 5, 10 and 20 mg/kg/day, IP), dopamine (GBR 12909, 5 mg/kg/day, IP) and noradrenaline (talsupram, 1, 5 and 10 mg/kg/day, IP). Citalopram and GBR 12909 did not modify the increased level of ethanol intake, but talsupram decreased ethanol intake to the levels seen prior to deprivation, and during the REM-rebound phase amplified the decrease found. These effects of talsupram could be antagonized by blocking mg/kg/day, IP). Prazosin alone tended to increase ethanol consumption. These findings suggest that functional alterations in central noradrenergic neurons during REM-sleep deprivation may contribute to the concurrent increase in ethanol intake.
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Acute sleep deprivation or chronic partial sleep restriction in animals often leads to enhanced risk taking and reward seeking, including cocaine and alcohol intake, sucrose self-administration, and intracranial self-stimulation.
“Acute sleep deprivation or chronic partial sleep restrictions in animals often leads to enhanced risk taking and reward seeking, including cocaine and alcohol intake, sucrose self-administration, as well as intra-cranial self-stimulations (99–103).”
From Impact of Sleep and Circadian Rhythms on Addiction Vulnerability in Adolescents (2018) · cites this paper as [99]
Animal studies have recapitulated the phenomenon of sleep loss-enhanced reward seeking observed in humans.
“animal studies have recapitulated the phenomenon of sleep loss-enhanced reward seeking observed in humans.”
From Impact of Sleep and Circadian Rhythms on Addiction Vulnerability in Adolescents (2018) · cites this paper as [99]
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Sleep deprivation amplifies striatal activation to monetary reward
Mullin, B. C., Phillips, M. L., Siegle, G. J., Buysse, D. J., Forbes, E. E., & Franzen, P. L. (2013) · Psychological Medicine · doi:10.1017/s0033291712002875 · Cited by 120 · see citing works
- Authors
- Aalto, J., & Kiianmaa, K.
- Venue
- Alcohol
- Publisher
- Elsevier BV
- Published
- 1986-11
- Volume
- 3
- Issue
- 6
- Pages
- 377-381
- ISSN
- 0741-8329 (ISSN-L)
- OpenAlex
- W2066239765
- Cited by
- 21
- References
- 17
- Citations by year
- 2026: 2 · 2023: 1 · 2022: 1 · 2021: 2 · 2019: 1 · 2017: 1 · 2016: 1 · 2014: 1 · 2013: 2
- FWCI
- 0.56
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Alcohol (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Health Sciences › Medicine › Epidemiology › Substance Abuse Treatment and Outcomes
- Keywords
- REM sleep deprivation, ethanol consumption, monoaminergic neurons, noradrenergic neurons, serotonin, dopamine, prazosin, citalopram, GBR 12909, REM rebound, alcohol consumption
- MeSH terms
- Alcohol Drinking, Animals, Biogenic Amines, Brain, Male, Neurons, Rats, Inbred Strains, Sleep Deprivation, Sleep, REM, Rats
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