Serotonergic inhibition of light-induced fos protein expression and extracellular glutamate in the suprachiasmatic nuclei

Selim, Magdi; Glass, John D.; Hauser, Ursula; Rea, Michael A.

doi:10.1016/0006-8993(93)90105-v

Cited by 107 publications

(41 citation statements)

References 35 publications

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“…Although substantial work has suggested a role for SCN 5HT in the generation of circadian rhythms (Levine et al 1986, Smale et al 1990, Medanic & Gillette 1992, Morin 1992, Possidente et al 1992, Prosser et al 1992, Selim et al 1993, the data reported here do not support such a relationship. There was a diurnal rhythm of serotonergic activity in the SCN only in DIE females in which 5HT was elevated during the light.…”

Section: Lh and Fshcontrasting

confidence: 99%

“…; 27,907·2; Aldrich Chemical Co., Milwaukee, WI, USA), or methysergide (a 5HT antagonist with dopaminergic actions; 3 mg/kg BW, i.p. ; Sandoz Pharmaceuticals, East Hanover, NJ, USA) at both 1100 and 1500 h. The dose of quipazine used here is the same as that employed to reduce LH levels in female rats (Lynch et al 1984) and slightly higher than that used to reduce light-induced fos expression in the SCN of male Syrian hamsters (12·5 mg/kg; (Selim et al 1993)). The doses of cyproheptadine and methysergide are the same as those used to inhibit ovulation (Markó & Flückiger 1980, Walker 1980 and LH secretion (Walker 1980) in proestrous rats.…”

Section: Methodsmentioning

confidence: 99%

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The neuroendocrine control of clock-timed gonadotropin release in the female Syrian hamster: role of serotonin

Ogilvie

Stetson²

1997

Journal of Endocrinology

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We hypothesized that rhythms in hypothalamic serotonergic activity were permissive to daily and estrous cyclerelated rhythms of LH, FSH and prolactin (PRL). In the Syrian hamster, proestrus (PRO) is characterized by a surge of LH, FSH and PRL; diestrus (DIE) by low LH and FSH and a small surge of PRL, while in photoperiodinduced anestrous (PIA) animals there is a surge of LH and FSH and low PRL. Turnover rates of serotonin (5HT) in four brain areas were determined for the three reproductive states at 2-h intervals. Turnover in the preoptic area and arcuate nuclei did not change, indicating that 5HT projections to these regions probably do not control LH, FSH or PRL release. Serotonin turnover in the median eminence (ME) was elevated at 0600 h in PIA females, at 0600 h, 0800 h, and 1400 h on DIE and at 0600 h and 2200 h on PRO. Since the pattern of 5HT turnover in the ME is different during each of the three reproductive states, 5HT in this area is likely not crucial to the control of LH, FSH and PRL. Turnover of 5HT also did not change in the suprachiasmatic nuclei (SCN) of PRO or PIA animals. However, 5HT turnover rates in the SCN were elevated at 1200 h, 2000 h, and 2400 h on DIE. The correlation of high 5HT turnover in the SCN of DIE but not PRO and PIA animals suggested that elevated serotonergic activity in the SCN is part of the mechanism by which the gonadotropin surge is prevented on DIE. To test this, PRO and DIE hamsters were injected with 5HT receptor ligands. Administration of a 5HT agonist attenuated the PRO surge of LH and blocked the surge of PRL. In contrast, administration of two 5HT antagonists failed to elicit a surge of LH in DIE and phenobarbital-blocked PRO females, an indication that other mechanisms also contribute to inhibition of gonadotropin and PRL surges.

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Section: Lh and Fshcontrasting

confidence: 99%

Section: Methodsmentioning

confidence: 99%

The neuroendocrine control of clock-timed gonadotropin release in the female Syrian hamster: role of serotonin

Ogilvie

Stetson²

1997

Journal of Endocrinology

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“…For example, 5-HT is believed to regulate the phasic effects of light on circadian rhythms (Kennaway et al 1996;Meyer-Bernstein and Morin 1996;Prosser et al 1993;Selim et al 1993;Smale et al 1990). Also, fluoxetine-induced increases in serotonergic transmission decrease the duration of circadian periods (Possidente et al 1996), and serotonergic afferents to the suprachiasmatic nucleus are necessary to synchronize nonphotic activity cues into circadian patterns (Edgar et al 1997).…”

mentioning

confidence: 99%

CSF 5-HIAA and Nighttime Activity in Free-Ranging Primates

Mehlman

2000

Neuropsychopharmacology

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Men with low CNS serotonin turnover, as measured by cerebrospinal fluid 5-hydroxyindoleacetic acid : Sleep, serotonin, impulsivity, primate, aggression Psychiatric research suggests that a reduced turnover rate of serotonin in the central nervous system (CNS), as measured by cerebrospinal fluid (CSF) 5-hydroxyindoleacetic acid (5-HIAA), is a risk factor for impaired impulse control, violent behavior, and premature mortality from suicide and violence (Faustman et al. 1990;Kruesi et al. 1990;Lidberg et al. 1985;Linnoila et al. Received February 12, 1999; revised June 16, 1999; accepted August 20, 1999. Dr. P.T. Mehlman and Dr. G.C. Westergaard are to be considered as co-first authors whose names are interchangeable. Dr. Mehlman was the Principal Investigator when the study was designed, the data were collected and analyzed, and was the first author when this manuscript was originally submitted. Dr. Westergaard was the Principal Investigator when the manuscript was revised and resubmitted for publication in this journal. Virkkunen et al. 1994). Research using nonhuman primates has replicated and extended many of these findings (Higley et al. 1996a;Higley et al. 1992a;Higley et al. 1996b;Kaplan et al. 1994;Mehlman et al. 1995;Mehlman et al. 1994;Mehlman et al. 1997;Raleigh 1987;Raleigh et al. 1983a;Raleigh et al. 1983b;Raleigh et al. 1980;Raleigh and McGuire 1994). Further, this research has demonstrated that inter-individual differences in CSF 5-HIAA concentrations are stable across time and experimental settings and can be attributed to genetic and early environmental influences that produce lasting modifications in the CNS serotonin response (Higley et al. 1996b;Higley et al. 1994;Higley et al. 1996a).Serotonin-mediated behavioral deficits are thought to result in part from an inability to maintain a homeostatic response in a number of physiological systems (Virkkunen et al. 1989a;Virkkunen and Narvanen 1987;Virkkunen et al. 1994). Various lines of evidence indicate that central serotonin neurotransmission contributes to regulation of sleep-wake cycles and circadian activity patterns. For example, several decades of research has shown that the sleep-wake cycle is partially modulated by serotonin release from projections of the ralphe nuclei (Jacobs 1991;Jouvet 1974;Jouvet 1967;Koella 1985;Koella and Czicman 1966;Maeda et al. 1989;Puizillout et al. 1981). Further, administration of p-chlorophenylalanine (PCPA), which inhibits the synthesis of serotonin, causes a reduction in total sleep in the cat (Jouvet 1974), rat (Torda 1967), and monkey (Weitzman et al. 1968). Finally, experimentally induced lesions of the ralphe system lead to nerve terminal decreases in 5-HT and 5-HIAA which are directly proportional to the degree of insomnia produced by the lesions (Jouvet 1974). These findings support the view that increases in CNS serotonin turnover rate promote sleep, in particular NREM sleep, and that deficits in serotonergic transmission are associated with insomnia, high levels of nighttime activity and/or...

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“…Serotonergic agents have been described as blocking the photic induction of Fos in the vSCN, suggesting a modulatory role of serotonin innervation to the nucleus. In hamsters, light-induced Fos expression at CT 7 was blocked by the nonspecific serotonin agonist quipazine (Selim et al 1993). In other hamster studies, 8-OH-DPAT, buspirone, the serotonin releaser fenfluramine, or the monoamine oxidase inhibitor harmaline given 7 hours after lights off (equivalent to CT 19 in the studies conducted for this work) inhibits the intense Fos expression induced by light in the vSCN.…”

Section: Discussionmentioning

confidence: 58%

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

Mullins

Gianutsos

1999

Neuropsychopharmacology

147

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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Serotonergic inhibition of light-induced fos protein expression and extracellular glutamate in the suprachiasmatic nuclei

Cited by 107 publications

References 35 publications

The neuroendocrine control of clock-timed gonadotropin release in the female Syrian hamster: role of serotonin

The neuroendocrine control of clock-timed gonadotropin release in the female Syrian hamster: role of serotonin

CSF 5-HIAA and Nighttime Activity in Free-Ranging Primates

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

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