c-fos mRNA in the suprachiasmatic nuclei in vitro shows a circadian rhythm and responds to a serotonergic agonist

Prosser, Rebecca A.; MacDonald, E; Heller, H. Craig

doi:10.1016/0169-328x(94)90292-5

Cited by 36 publications

(18 citation statements)

References 50 publications

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“…Previous work has demonstrated that exercise and forced arousal in the subjective day significantly attenuate FOS-ir in the hamster SCN Mikkelsen et al, 1998). Quipazine also suppresses c-Fos expression in the subjective day in the rat SCN in vitro (Prosser et al, 1994) but has been reported to induce expression in the subjective night in rat SCN in vivo, again mimicking effects of light (Kohler et al, 1999;Moyer et al, 1997;Neumaier et al, 2001). Our data support the evidence for species differences but define a different pattern of responses.…”

Section: C-fos Immunoreactivitysupporting

confidence: 88%

“…5-HT at this time of day can induce large phase-advance shifts of the circadian rhythm of firing rates of rat and Syrian hamster SCN neurons in vitro, most likely by actions at 5-HT 7 receptors (Gannon, 2001;Prosser, 2000). Basal c-Fos mRNA expression in the SCN in vitro is suppressed by 5-HT agonists at this time (Prosser et al, 1994). In vivo, 5-HT 1A/7 agonists, applied systemically, can induce phase shifts of behavioral rhythms in the rat and hamster.…”

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confidence: 94%

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Response of the Mouse Circadian System to Serotonin 1A/2/7 Agonists in vivo: Surprisingly Little

et al. 2003

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Serotonin (5-HT) is thought to play a role in regulating nonphotic phase shifts and modulating photic phase shifts of the mammalian circadian system, but results with different species (rats vs. hamsters) and techniques (in vivo vs. in vitro; systemic vs. intracerebral drug delivery) have been discordant. Here we examined the effects of the 5-HT1A/7 agonist 8-OH-DPAT and the 5-HT1/2 agonist quipazine on the circadian system in mice, with some parallel experiments conducted with hamsters for comparative purposes. In mice, neither drug, delivered systemically at a range of circadian phases and doses, induced phase shifts significantly different from vehicle injections. In hamsters, quipazine intraperitoneally (i.p.) did not induce phase shifts, whereas 8-OH-DPAT induced phase shifts after i.p. but not intra-SCN injections. In mice, quipazine modestly increased c-Fos expression in the SCN (site of the circadian pacemaker) during the subjective day, whereas 8-OH-DPAT did not affect SCN c-Fos. In hamsters, both drugs suppressed SCN c-Fos in the subjective day. In both species, both drugs strongly induced c-Fos in the paraventricular nucleus (within-subject positive control). 8-OH-DPAT did not significantly attenuate light-induced phase shifts in mice but did in hamsters (between-species positive control). These results indicate that in the intact mouse in vivo, acute activation of 5-HT1A/2/7 receptors in the circadian system is not sufficient to reset the SCN pacemaker or to oppose phase-shifting effects of light. There appear to be significant species differences in the susceptibility of the circadian system to modulation by systemically delivered serotonergics.

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Section: C-fos Immunoreactivitysupporting

confidence: 88%

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confidence: 94%

Response of the Mouse Circadian System to Serotonin 1A/2/7 Agonists in vivo: Surprisingly Little

et al. 2003

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“…Fos protein in the SCN, for example, oscillates in the absence of photoperiodic time cues (Earnest et al 1992). The same is true for the respective mRNA in vitro (Prosser et al 1994). Parallel to fos, the expression of the period repeat sequence continues during constant darkness (Matsui et al 1993).…”

Section: Endogenous Oscillations Of the Scnmentioning

confidence: 56%

Components and connections of the circadian timing system in mammals

Reuss

1996

Cell and Tissue Research

102

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The circadian timing system is a neural network consisting of the hypothalamic suprachiasmatic nucleus, aided by the retina, other hypothalamic nuclei, autonomic regions of the spinal cord, sympathetic ganglia and the pineal gland. Extensive studies conducted over the last two decades have unravelled the principal items of its functional neuroanatomy. The system is responsible for the generation of the circadian rhythm, its synchronization by environmental factors such as light, and its mediation with respect to morphological, physiological and biochemical parameters of mammals that exhibit distinct alterations throughout the 24-h cycle. This review characterizes the brain sites involved and the pathways responsible for the generation and maintenance of circadian rhythmicity.

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“…However, the transcriptional activation of several circadian-regulated genes (vasopressin, brain-derived neurotrophic factor, Fos; Refs. [22][23][24] requires complex interactions of several different classes of enhancer elements (25)(26)(27), suggesting the involvement of different transcription pathways in circadian gene regulation within the SCN. The elucidation of these pathways will provide valuable insight into the series of coordinated transcriptional events underlying circadian rhythmicity.…”

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confidence: 99%

Circadian Regulation of cAMP Response Element-mediated Gene Expression in the Suprachiasmatic Nuclei

Obrietan¹,

Impey

Smith

et al. 1999

Journal of Biological Chemistry

261

197

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A program of stringently-regulated gene expression is thought to be a fundamental component of the circadian clock. Although recent work has implicated a role for E-box-dependent transcription in circadian rhythmicity, the contribution of other enhancer elements has yet to be assessed. Here, we report that cells of the suprachiasmatic nuclei (SCN) exhibit a prominent circadian oscillation in cAMP response element (CRE)-mediated gene expression. Maximal reporter gene expression occurred from late-subjective night to mid-subjective day. Cycling of CRE-dependent transcription was not observed in other brain regions, including the supraoptic nucleus and piriform cortex. Levels of the phospho-active form of the transcription factor CREB (P-CREB) varied as a function of circadian time. Peak P-CREB levels occurred during the mid-to late-subjective night. Furthermore, photic stimulation during the subjective night, but not during the subjective day, triggered a marked increase in CRE-mediated gene expression in the SCN. Reporter gene experiments showed that activation of the p44/42 mitogen-activated protein kinase signaling cascade is required for Ca 2؉ -dependent stimulation of CRE-mediated transcription in the SCN. These findings reveal the CREB/CRE transcriptional pathway to be circadian-regulated within the SCN, and raise the possibility that this pathway provides signaling information essential for normal clock function.

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c-fos mRNA in the suprachiasmatic nuclei in vitro shows a circadian rhythm and responds to a serotonergic agonist

Cited by 36 publications

References 50 publications

Response of the Mouse Circadian System to Serotonin 1A/2/7 Agonists in vivo: Surprisingly Little

Response of the Mouse Circadian System to Serotonin 1A/2/7 Agonists in vivo: Surprisingly Little

Components and connections of the circadian timing system in mammals

Circadian Regulation of cAMP Response Element-mediated Gene Expression in the Suprachiasmatic Nuclei

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