Chronic ethanol intake modulates photic and non-photic circadian phase responses in the Syrian hamster

Seggio, Joseph A.; Logan, Ryan W.; Rosenwasser, Alan M.

doi:10.1016/j.pbb.2007.05.001

Cited by 38 publications

(44 citation statements)

References 43 publications

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“…This result is largely consistent with a previous study in chronically drinking hamsters where EtOH inhibited photic advances but not delays (81). The basis of this differential effect of EtOH on phase resetting is not clear but could reflect a distinct inhibitory action directed at a component of the intracellular photic clock-resetting pathway devoted to phase-advance shifting.…”

Section: Discussionsupporting

confidence: 91%

“…In hamsters, for example, chronic drinking is reported to have minor effects on circadian rhythm stability and period characteristics and does not impede the rate of reentrainment to a shifted LD cycle (51). On the other hand, chronic EtOH has been shown reduce light pulse-induced phase advances (but not phase delays) and inhibit phase advance shifts to triazolam (81). In rats, chronic EtOH alters the free-running period under DD but apparently has no effect on photic phase resetting (77,78).…”

Section: Discussionmentioning

confidence: 99%

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Acute ethanol impairs photic and nonphotic circadian phase resetting in the Syrian hamster

Ruby

Prosser²,

DePaul³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Disrupted circadian rhythmicity is associated with ethanol (EtOH) abuse, yet little is known about how EtOH affects the mammalian circadian clock of the suprachiasmatic nucleus (SCN). Clock timing is regulated by photic and nonphotic inputs to the SCN involving glutamate release from the retinohypothalamic tract and serotonin (5-HT) from the midbrain raphe, respectively. Our recent in vitro studies in the SCN slice revealed that EtOH blocks photic phase-resetting action of glutamate and enhances the nonphotic phase-resetting action of the 5-HT1A,7 agonist, 8-OH-DPAT. To explore the basis of these effects in the whole animal, we used microdialysis to characterize the pharmacokinetics of intraperitoneal injection of EtOH in the hamster SCN extracellular fluid compartment and then studied the effects of such EtOH treatment on photic and serotonergic phase resetting of the circadian locomotor activity rhythm. Peak EtOH levels (approximately 50 mM) from a 2 g/kg injection occurred within 20-40 min with a half-life of approximately 3 h. EtOH treatment dose-dependently attenuated photic phase advances but had no effect on phase delays and, contrary to in vitro findings, markedly attenuated 8-OH-DPAT-induced phase advances. In a complementary experiment using reverse microdialysis to deliver a timed SCN perfusion of EtOH during a phase-advancing light pulse, the phase advances were blocked, similar to systemic EtOH treatment. These results are evidence that acute EtOH significantly affects photic and nonphotic phase-resetting responses critical to circadian clock regulation. Notably, EtOH inhibition of photic signaling is manifest through direct action in the SCN. Such actions could underlie the disruption of circadian rhythmicity associated with alcohol abuse.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Acute ethanol impairs photic and nonphotic circadian phase resetting in the Syrian hamster

Ruby

Prosser²,

DePaul³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

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“…For example, the number of neurons containing vasopressin, vasoactive intestinal polypeptide, and several other neuropeptides in the SCN was shown to be decreased after chronic alcohol (Madeira et al, 1997). Chronic alcohol also disrupts the responsiveness of the SCN to both photic and nonphotic phase resetting (Seggio et al, 2007). In addition, under constant conditions without the strong Zeitgeber of light, chronic alcohol shortens the periodicity of wheel-running behaviors (Seggio et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

Chronic Alcohol Consumption in Rats Leads to Desynchrony in Diurnal Rhythms and Molecular Clocks

Guo

Simasko

Jansen

2016

Alcoholism Clin & Exp Res

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Our findings suggest that desynchrony among internal rhythms is an important and overlooked aspect of alcohol-induced circadian disruptions. The misalignment of phases among rhythms may compromise normal physiological functions and put individuals with chronic alcohol use at greater risk for developing other physical and mental health issues. How this desynchrony occurs and the extent to which it participates in alcohol-related pathologies requires further investigation.

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“…For example, chronic ethanol in hamsters apparently does not alter circadian clock re-entrainment (Mistlberger and Nadeau, 1992), while chronic ethanol can inhibit light-induced phase advances and (daytime) triazolam-induced phase advances in hamsters, but not light-induced phase delays (Seggio et al, 2007). Rosenwasser, et al (2005a,b) also showed that chronic ethanol affects circadian free-running periods in rats but not light-induced phase shifts.…”

Section: Discussion Ethanol Blocks Glutamate-induced Phase Shiftsmentioning

confidence: 99%

“…(Reid and Zee, 2004). Recent studies show that chronic ethanol alters the circadian free-running period in rats (Rosenwasser et al, 2005a,b) and inhibits light-and triazolam-induced phase shifts in hamsters (Seggio et al, 2007). However, little work has focused on whether acute ethanol affects circadian rhythms, and whether such effects involve direct actions on the master circadian clock located in the suprachiasmatic nucleus (SCN).…”

mentioning

confidence: 99%

Acute ethanol modulates glutamatergic and serotonergic phase shifts of the mouse circadian clock in vitro

2008

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Alcohol abuse is associated with sleep problems, which are often linked to circadian rhythm disturbances. However, there is no information on the direct effects of ethanol on the mammalian circadian clock. Acute ethanol inhibits glutamate signaling, which is the primary mechanism through which light resets the mammalian clock in the suprachiasmatic nucleus (SCN). Glutamate and light also inhibit circadian clock resetting induced by non-photic signals, including serotonin. Thus, we investigated the effects of acute ethanol on both glutamatergic and serotoninergic resetting of the SCN clock in vitro. We show that ethanol dose-dependently inhibits glutamate-induced phase shifts and enhances serotonergic phase shifts. The inhibition of glutamate-induced phase shifts is not affected by excess glutamate, glycine or D-serine, but is prevented by excess brain-derived neurotrophic factor (BDNF). BDNF is known to augment glutamate signaling in the SCN and to be necessary for glutamate/light-induced phase shifts. Thus, ethanol may inhibit glutamate-induced clock resetting at least in part by blocking BDNF enhancement of glutamate signaling. Ethanol enhancement of serotonergic phase shifts is mimicked by treatments that suppress glutamate signaling in the SCN, including antagonists of glutamate receptors, BDNF signaling and nitric oxide synthase. The combined effect of ethanol with these treatments is not additive, suggesting they act through a common pathway. Our data indicate further that the interaction between serotonin and glutamate in the SCN may occur downstream from nitric oxide synthase activation. Thus, acute ethanol disrupts normal circadian clock phase regulation, which could contribute to the physiological and psychological problems associated with alcohol abuse. Keywords suprachiasmatic nucleus; circadian rhythms; ethanol; glutamate; serotonin; brain-derived neurotrophic factorThe development of alcoholism and the likelihood of relapse drinking are associated with poor sleep quality and the deleterious effects of ethanol on sleep (Landolt and Gillin, 2001;Brower et al., 2001). Alcohol consumption reduces sleep quality (Kubota et al., 2002;Ehler and Slawecki, 2000;Landolt et al., 1996), which is closely linked to the circadian system. For example, the inability to fall asleep at the desired time can result from improper synchronization *Corresponding author: Dept. Biochemistry and Cellular and Molecular Biology, University of Tennessee, Knoxville, TN 37996, phone: (865) 974-2722, FAX: (865)-974-6306, rprosser@utk.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal per...

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Chronic ethanol intake modulates photic and non-photic circadian phase responses in the Syrian hamster

Cited by 38 publications

References 43 publications

Acute ethanol impairs photic and nonphotic circadian phase resetting in the Syrian hamster

Acute ethanol impairs photic and nonphotic circadian phase resetting in the Syrian hamster

Chronic Alcohol Consumption in Rats Leads to Desynchrony in Diurnal Rhythms and Molecular Clocks

Acute ethanol modulates glutamatergic and serotonergic phase shifts of the mouse circadian clock in vitro

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