Melatonin influences Fos expression in the rat suprachiasmatic

Kilduff, Thomas S.; Landel, Hollister B.; Nagy, Gabriella; Sutin, Ellen L.; Dement, William C.; Heller, H. Craig

doi:10.1016/0169-328x(92)90192-e

Cited by 47 publications

(17 citation statements)

References 29 publications

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“…Melatonin has been shown to inhibit forskolin-stimulated induction of c-fos and junB mRNA as well as c-Fos protein in ovine pars tuberalis cells (37) and to inhibit GnRH-induced c-Fos immunoreactivity in neonatal rat pituitary cells (8). The only tissue in which melatonin has been shown to increase c-fos immediate early gene expression is the rat SCN (38). We have shown that melatonin induces a rapid but transient increase in both c-fos and junB mRNA expression in the GT1-7 cells.…”

Section: Discussionmentioning

confidence: 69%

“…In the neonatal rat pituitary and ovine pars tuberalis, melatonin down-regulates c-fos mRNA and protein expression (8,37). In the rat SCN, melatonin either induces or has no effect on c-fos mRNA expression (38,39). To determine whether melatonin induced immediate early gene expression in GT1-7 cells, we used Northern blot analysis to examine c-fos and junB mRNA expression.…”

Section: Melatonin Receptors In Gt1-7 Cells Are Coupled To G I/o Protmentioning

confidence: 99%

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Melatonin Receptor Activation Regulates GnRH Gene Expression and Secretion in GT1–7 GnRH Neurons

Roy¹,

Belsham²

2002

Journal of Biological Chemistry

129

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Melatonin plays a significant role in the control of the hypothalamic-pituitary-gonadal axis. Using the GT1-7 cell line, an in vitro model of GnRH-secreting neurons of the hypothalamus, we examined the potential signal transduction pathways activated by melatonin directly at the level of the GT1-7 neuron. We found that melatonin inhibits forskolin-stimulated adenosine 3-, 5-cyclic monophosphate accumulation in GT1-7 cells through an inhibitory G protein. Melatonin induced protein kinase C activity by 1.65-fold over basal levels, increased the phosphorylation of extracellular signal-regulated kinase 1 and 2 proteins, and activated c-fos and junB mRNA expression in GT1-7 cells. Using the protein kinase A inhibitor H-89, the protein kinase C inhibitor bisindolylmaleimide, and the mitogen-activated protein kinase kinase inhibitor PD98059, we found that the melatonin-mediated cyclical regulation of GnRH mRNA expression may involve the protein kinase C and the extracellular signal-regulated kinase 1 and 2 pathways, but not the protein kinase A pathway. We found that melatonin suppresses GnRH secretion by ϳ45% in the GT1-7 neurons. However, in the presence of the inhibitors H-89, bisindolylmaleimide, and PD98059 melatonin was unable to suppress GnRH secretion. These results provide insights into the potential signal transduction mechanisms involved in the control of GnRH gene expression and secretion by melatonin.

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Section: Discussionmentioning

confidence: 69%

Section: Melatonin Receptors In Gt1-7 Cells Are Coupled To G I/o Protmentioning

confidence: 99%

Melatonin Receptor Activation Regulates GnRH Gene Expression and Secretion in GT1–7 GnRH Neurons

Roy¹,

Belsham²

2002

Journal of Biological Chemistry

129

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“…Highly significant damping of glucose utilization was observed after stimulation in late subjective daytime (CT 6 and 10), whereas a modest, but significant, enhancement was observed in the subjective predawn period (CT 22). More recently, intraperitoneal melatonin injections that preceded subjective dawn (CT 23), but not at other times including subjective predusk of rats continuously in the dark, were reported to induce immunoreactivity for the immediate-early gene product, Fos, in SCN [ 14].…”

Section: Circadian Changes In Acute Responses Of Scn Physiology To Mementioning

confidence: 99%

Circadian actions of melatonin at the suprachiasmatic nucleus

Gillette

McArthur

1995

Behavioural Brain Research

110

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The biological clock in the suprachiasmatic nucleus (SCN) of the hypothalamus plays a well-defined role in regulating melatonin production by the pineal. Emerging evidence indicates that melatonin itself can feed back upon the SCN and thereby influence circadian functions. Melatonin administration has been shown to entrain activity rhythms in rodents and humans. Melatonin binds specifically within the SCN and alters SCN physiology by both acute and clock-resetting mechanisms. The circadian clock in the SCN appears to temporally restrict its own sensitivity to melatonin, such that physiological sensitivity is greatest in the subjective dusk period

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“…3 Effects of Antidepressants 363 SCN neurons. Several investigations have demonstrated that Fos protein expression is involved in lightinduced entrainment mechanisms (Ginty et al 1993;Kilduff et al 1992;Moore 1995). Furthermore, induction of Fos expression is anatomically specific and exclusively occurs in response to phase-shifting stimuli in the ventrolateral portion of the SCN (Ginty et al 1993;Moore 1995;Miller et al 1996).…”

Section: Discussionmentioning

confidence: 99%

“…Receptor-mediated IEG expression and Fos protein deposition in the vSCN occurs during stimulus-specific circadian times in response to such phase-shifting stimuli as light and melatonin receptor stimulation (Ginty et al 1993;Kilduff et al 1992;Kornhauser et al 1992;Mullins et al 1999;Sutin and Kilduff 1992). It has been shown that in the SCN, CREB is phosphorylated by light exposure only at the circadian times when Fos expression is induced and the SCN has been activated, an effect that corresponds directly with phase shifts of locomotor activity (Ginty et al 1993).…”

mentioning

confidence: 99%

Effects of Antidepressants on 5-HT7 Receptor Regulation in the Rat Hypothalamus

Mullins

Gianutsos

1999

Neuropsychopharmacology

148

101

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Recent evidence suggests that a novel serotonin receptor 5-HT 7 localized in the hypothalamus downregulates in response to treatment with the antidepressant fluoxetine (Sleight et al. 1995). This receptor has also been implicated in the regulation of circadian rhythms (Lovenberg et al. 1993). Here Depression may involve many possible abnormalities corresponding to multiple biological correlates of dysfunction or dysregulation in either one or several brain neurotransmitter systems (Cooper et al. 1996;Nair and Sharma 1989), a property that may contribute to the apparent disparity in symptomology and response to antidepressant therapy. The strict classical notions of neurotransmitter dysregulation hypotheses that associate depression with a deficiency of a vailable neurotransmitter or subresponsivity of mainly noradrenergic and/ or serotonergic receptor systems are recently being expanded to include disturbances in biological rhythm regulation. Impairment of the efficiency of rhythm maintenance or rhythm desynchronization has been suggested by many to lead to mental fatigue and depression (Goodwin et al. 1982;Hallonquist et al. 1986;Healy 1987;Partonen 1994;Schwartz 1993;Wirz-Justice and Campbell 1982;Wirz-Justice et al. 1995). Clinically, it has been extensively documented that the timing and structure of rhythms in physiological, behavioral, and endocrinological functions seem to be abnormal in depression (Coiro et al. 1993;Duncan 1996;File 1990;Kupfer 1995;Nair and Sharma 1989;Wehr et al. 1979). Furthermore, studies investigating the patterns of circadian rhythms of patients diagnosed with depression have been undertaken with the premise of disturbed rhythmicity as a central theme underlying the etiology of some affective disorders (Duncan 1996;Goodwin et al. 1982;Healy 1987;Siever and Davis, 1985;Souetre et al. 1988).Although melatonin is generally thought to be a primary modulator of circadian function through the suprachiasmatic nucleus (SCN) of the hypothalamus (Armstrong and Redman 1993;Binkley 1993;Cassone et al. 1993;Dubocovich 1991;Ibata et al. 1997;Reiter 1993; From the Bristol-Myers Squibb Company (ULM, ASE), Neuroscience Drug Discovery, Wallingford, Connecticut; and University of Connecticut, Department of Pharmaceutical Sciences (GG), Storrs, Connecticut, USA.Address correspondence to: U. Lena Mullins, Ph.D., BristolMyers Squibb Company, Neuroscience Drug Discovery, Department 408, 5 Research Parkway, Wallingford, Connecticut 06492, USA.Received January 1, 1999; revised March 23, 1999; accepted March 26, 1999. N EUROPSYCHOPHARMACOLOGY 1999 -VOL . 21 , NO . 3 Effects of Antidepressants 353 Stankov et al. 1993), the serotonergic system also plays a critical role in circadian modulation. The SCN receives dense projections from the raphe serotonergic neurons originating in the brainstem (Jacobs and Azmitia 1992;Meyer-Bornstein and Morin 1996;Van De Kar and Lorens 1979). Lesions of the median raphe serotonergic system using the neurotoxic agent 5,7-dihydroxytryptamine (5,7-DHT) produce a sever...

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Melatonin influences Fos expression in the rat suprachiasmatic

Cited by 47 publications

References 29 publications

Melatonin Receptor Activation Regulates GnRH Gene Expression and Secretion in GT1–7 GnRH Neurons

Melatonin Receptor Activation Regulates GnRH Gene Expression and Secretion in GT1–7 GnRH Neurons

Circadian actions of melatonin at the suprachiasmatic nucleus

Effects of Antidepressants on 5-HT7 Receptor Regulation in the Rat Hypothalamus

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