Neuropeptide y and behaviorally induced phase shifts

Biello, Stephany M.; Janik, Daniel S.; Mrosovsky, N.

doi:10.1016/0306-4522(94)90331-x

Cited by 187 publications

(117 citation statements)

References 22 publications

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“…Studies in animals have indicated that the possible neuroanatomical pathway for non-photic stimuli to affect the circadian pacemaker may include the intergeniculate leaflet, which can transfer non-photic information to the suprachiasmatic nucleus (SCN) via neuropeptide-Y (Biello et al, 1994;Lewandowski and Usarek, 2002). These studies do not differentiate between behavioral state (i.e.…”

Section: The Effects Of Non-photic Stimuli On the Mammalian Circadianmentioning

confidence: 99%

Addition of a non-photic component to a light-based mathematical model of the human circadian pacemaker

Hilaire

Klerman

Khalsa

et al. 2007

Journal of Theoretical Biology

145

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Mathematical models have become vital to the study of many biological processes in humans due to the complexity of the physiological mechanisms underlying these processes and systems. While our current mathematical representation of the human circadian pacemaker has proven useful in many experimental situations, it uses as input only a direct effect of light on the circadian pacemaker. Although light (a photic stimulus) has been shown to be the primary synchronizer of the circadian pacemaker across a number of species, studies in both animals and humans have confirmed the existence of non-photic effects that also contribute to phase shifting and entrainment. We modified our light-based circadian mathematical model to reflect evidence from these studies that the sleep-wake cycle and/or associated behaviors have a non-photic effect on the circadian pacemaker. In our representation, the sleep-wake cycle and its associated behaviors provides a non-photic drive on the pacemaker that acts both independently and concomitantly with light stimuli. Further experiments are required to validate fully our model and to understand the exact effect of the sleep-wake cycle as a non-photic stimulus for the human circadian pacemaker.

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Section: The Effects Of Non-photic Stimuli On the Mammalian Circadianmentioning

confidence: 99%

Addition of a non-photic component to a light-based mathematical model of the human circadian pacemaker

Hilaire

Klerman

Khalsa

et al. 2007

Journal of Theoretical Biology

145

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“…These results constitute strong evidence that the IGL is necessary for entrainment to daily activity schedules in mice. Studies of hamsters have shown that intraventricular injections of NPY can cause phase shifts similar in timing and magnitude to those produced by scheduled bouts of wheel running (Albers and Ferris, 1984;Biello et al, 1994;Huhman and Albers, 1994) and that shifts in response to bouts of running can be blocked by injections of NPY-antibody into the SCN area (Biello et al, 1994). In addition, running activity induces Fos protein in the IGL, which colocalizes with NPY (Janik et al, 1995).…”

Section: Strong Evidence That Npy Mediates Entrainment By Activitymentioning

confidence: 99%

Both Neuropeptide Y and Serotonin Are Necessary for Entrainment of Circadian Rhythms in Mice by Daily Treadmill Running Schedules

1997

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This study investigated the role of the suprachiasmatic nucleus (SCN) circadian pacemaker and its neuropeptide Y (NPY) and serotonin (5-HT) afferents in entrainment (synchronization) of mouse circadian rhythms by treadmill running. Blind C57BL/6j mice were run in treadmills for 3 hr/d for 3-10 weeks after receiving radio-frequency lesions of the SCN or the intergeniculate leaflet (IGL, the source of SCN NPY) or infusions of the 5-HT neurotoxin 5,7-DHT into the SCN area. Of 25 intact mice, 22 entrained and three showed period (, the mean duration of the circadian cycle) modulations to scheduled running. Arrhythmic SCN-ablated mice did not synchronize to scheduled running in a way suggestive of circadian pacemaker mediation. Of 15 mice with IGL lesions, only two with partial lesions entrained. Mice with complete IGL lesions (five), confirmed by immunocytochemistry, showed no entrainment or changes. Of 19 mice with 5-HT lesions, only two with partial lesions entrained. All but two mice with complete (10) or nearly complete (4) 5-HT denervation, confirmed by immunocytochemistry, showed modulations during the treadmill schedule. Failure to entrain was not explained by group differences in before the treadmill schedules. The results indicate that the SCN and both NPY and 5-HT are necessary for entrainment to 24 hr schedules of forced running but that complete loss of 5-HT does not prevent modulations of pacemaker motion by behavioral stimuli. Treadmill entrainment in mice may involve synergistic interactions between 5-HT and NPY afferents at some site within the circadian system.

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“…Arousal or behavioral activity during the daytime (for nocturnal rodents) induce robust phase advances (Mrosovsky, 1988;Reebs et al, 1989;Antle and Mistlberger, 2000) that may involve neuropeptide Y (Biello et al, 1994;Golombek et al, 1996;Marchant et al, 1997) and/or serotonin (5-HT) (Prosser, 2003;Tominaga et al, 1992;Horikawa and Shibata, 2004;Marchant et al, 1997;Glass et al, 2003) signaling in the SCN. Interestingly, acute ethanol alters serotonergic signaling (Hayashi et al, 2003;Thielen et al, 2002;Daws et al, 2006), raising the possibility that ethanol could also affect the circadian system through modulating serotonergic signaling.…”

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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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Neuropeptide y and behaviorally induced phase shifts

Cited by 187 publications

References 22 publications

Addition of a non-photic component to a light-based mathematical model of the human circadian pacemaker

Addition of a non-photic component to a light-based mathematical model of the human circadian pacemaker

Both Neuropeptide Y and Serotonin Are Necessary for Entrainment of Circadian Rhythms in Mice by Daily Treadmill Running Schedules

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

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