Sleep deprivation stimulates serotonin release in the suprachiasmatic nucleus

Gh, Grossman; Re, Mistlberger; Antle, MC; Ehlen, J. Christopher; Jd, Glass

doi:10.1097/00001756-200006260-00024

Cited by 85 publications

(63 citation statements)

References 12 publications

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“…Furthermore, like antidepressant treatment, TSD in rats stimulates hippocampal neurogenesis (Grassi Zucconi et al, 2006). It has also been shown in hamsters that TSD affects serotonin levels in the SCN and other brain regions, and results in a strong phase advance in activity rhythms (Asikainen et al, 1995;Grossman et al, 2000). These studies are just beginning, and are important in determining the mechanism underlying the therapeutic effects of TSD as an antidepressant.…”

Section: Treating Mood Disorders By Altering the Circadian Cycle 41 mentioning

confidence: 96%

Circadian genes, rhythms and the biology of mood disorders

McClung

2007

Pharmacology & Therapeutics

576

386

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For many years, researchers have suggested that abnormalities in circadian rhythms may underlie the development of mood disorders such as bipolar disorder, major depression and seasonal affective disorder. Furthermore, some of the treatments that are currently employed to treat mood disorders are thought to act by shifting or "resetting" the circadian clock, including total sleep deprivation and bright light therapy. There is also reason to suspect that many of the mood stabilizers and antidepressants used to treat these disorders may derive at least some of their therapeutic efficacy by affecting the circadian clock. Recent genetic, molecular and behavioral studies implicate individual genes that make up the clock in mood regulation. As well, important functions of these genes in brain regions and neurotransmitter systems associated with mood regulation is becoming apparent. In this review, the evidence linking circadian rhythms and mood disorders, and what is known about the underlying biology of this association, is presented.

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Section: Treating Mood Disorders By Altering the Circadian Cycle 41 mentioning

confidence: 96%

Circadian genes, rhythms and the biology of mood disorders

McClung

2007

Pharmacology & Therapeutics

576

386

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“…It is well established that light and glutamate agonists inhibit non-photic phase shifts (Mrosovsky, 1991;Grossman et al, 2000;Hall et al, 1999;Gamble et al, 2004;Biello et al, 1997;Prosser, 2001). Further, we have shown that non-photic phase shifts, including in vitro serotonergic phase shifts, are enhanced by a treatment (enzymatic removal of polysialic acid) that inhibits glutamate signaling in the SCN (Fedorkova et al, 2002).…”

Section: Ethanol Enhancement Of Serotonergic Phase Shifts Could Occurmentioning

confidence: 99%

“…Moreover, there is a mutually antagonistic relationship between non-photic stimuli that induce daytime phase shifts and photic input mediating nighttime phase shifts. Light or glutamate stimulation during the day inhibits non-photic phase shifts (Mrosovsky, 1991;Grossman et al, 2000;Hall et al, 1999;Gamble et al, 2004;Biello et al, 1997;Prosser, 2001;Kallingal and Mintz, 2007), while nighttime presentation of non-photic stimuli suppresses light/glutamate-induced phase shifts (Ralph and Mrosovsky, 1992;Yannielli and Harrington, 2004;Smith et al, 2001;Gamble et al, 2004;Biello et al, 1997;Kallingal and Mintz, 2007). Conversely, suppressing glutamate signaling during the day can enhance phase shifts induced by non-photic stimuli (Fedorkova et al, 2002), while decreasing neuropeptide Y or 5-HT signaling at night can enhance photic phase shifts (Yannielli and Harrington, 2004;Lall and Harrington, 2006;Smart and Biello, 2001;Muscat et al, 2005).…”

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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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“…The procedures used for sleep deprivation were similar to those used in a previous study (Grossman et al, 2000). Beginning at ZT 6, animals outfitted with a microdialysis probe in the SCN and an injection reentry cannula aimed at the DRN were aroused and maintained in the waking state in their home cage for 3 hr by continuous gentle handling and light puffs of air.…”

Section: Effects Of Intra-drn 5-ht Antagonists On Sleep Deprivation-imentioning

confidence: 99%

“…For example, there is evidence that 5-HT acts in the SCN to mediate the clock-resetting effects of behavioral stimulation. This includes findings that 5-HT agonists applied to the SCN in vitro or in vivo reset circadian phase (Prosser et al, 1990Medanic and Gillette, 1992;Challet et al, 1998;Ehlen et al, 2001) and that behavioral phaseresetting manipulations evoke SCN 5-HT release (Dudley et al, 1998;Grossman et al, 2000). Conversely, reports that raphe lesions (Meyer-Bernstein and Morin, 1998), treatment with 5-HT antagonists (Antle et al, 1998), or depletion of 5-HT in the SCN (Bobrzynska et al, 1996) do not block behavioral phase shifting argue against a role of 5-HT in circadian clock resetting.…”

Section: Introductionmentioning

confidence: 99%