title: The neuroendocrine control of clock-timed gonadotropin release in the female Syrian hamster: role of serotonin.
abstract: We hypothesized that rhythms in hypothalamic serotonergic activity were permissive to daily and estrous cycle-related 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 photoperiod-induced 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.
authors.affiliation: Department of Biology, University of Delaware, Newark 19716, USA.
authors.forename: K M
authors.initials: KM
authors.lastname: Ogilvie
authors.forename: M H
authors.initials: MH
authors.lastname: Stetson
mesh_terms: D000780:Anestrus / Q000097:blood; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism*; D006224:Cricetinae; D003533:Cyproheptadine / Q000494:pharmacology; D004031:Diestrus / Q000097:blood; D004971:Estrus / Q000097:blood*; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D006065:Gonadotropins, Pituitary / Q000097:blood*; D007986:Luteinizing Hormone / Q000097:blood; D008473:Median Eminence / Q000187:drug effects / Q000378:metabolism; D008647:Mesocricetus; D008784:Methysergide / Q000494:pharmacology; D008996:Monoamine Oxidase Inhibitors / Q000494:pharmacology; D010293:Pargyline / Q000494:pharmacology; D017440:Photoperiod; D011359:Proestrus / Q000097:blood; D011388:Prolactin / Q000097:blood; D011814:Quipazine / Q000494:pharmacology; D012701:Serotonin / Q000378:metabolism / Q000502:physiology*; D012702:Serotonin Antagonists / Q000494:pharmacology; D017366:Serotonin Receptor Agonists / Q000494:pharmacology; D013493:Suprachiasmatic Nucleus / Q000187:drug effects / Q000378:metabolism; D013997:Time Factors
chemical_list: D006065:Gonadotropins, Pituitary; D008996:Monoamine Oxidase Inhibitors; D012702:Serotonin Antagonists; D017366:Serotonin Receptor Agonists; D003533:Cyproheptadine; D012701:Serotonin; D011814:Quipazine; D011388:Prolactin; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D010293:Pargyline; D008784:Methysergide