title: Maintenance of gonadotropin secretion by glucocorticoids under stress conditions through the inhibition of prostaglandin synthesis in the brain.
abstract: We have previously reported that glucocorticoids counteract the suppressive effects of tumor necrosis factor-alpha on both pulsatile and surge secretion of LH. This suggests that glucocorticoids have a protective effect on reproductive function under infectious stress. In the present study, we examined whether glucocorticoids maintain pulsatile LH secretion under various conditions of acute stress and the possible involvement of prostaglandins (PGs) in glucocorticoid actions. Three different types of stressors, namely infectious (lipopolysaccharide, 0.5 microg/kg), hypoglycemic (2-deoxy-D-glucose, 100 mg/kg), and restraint stress (1 h) were applied to ovariectomized rats. In ovariectomized rats, LH pulses were partially suppressed by restraint, but not by lipopolysaccharide or 2-deoxy-D-glucose. On the other hand, adrenalectomy (ADX) significantly enhanced the suppressive effects of all the stressors applied on LH pulses. Treatment with both corticosterone (25 mg/kg) and indomethacin (10 mg/kg) in ADX rats significantly attenuated the suppressive effects of these stressors on LH pulses. In addition, the immunoreactivity of cyclooxygenase-2, a PG-synthesizing enzyme, in the brain under stress conditions was much enhanced by ADX, and this was counteracted by corticosterone treatment. Similarly, an increase in body temperature under restraint stress was enhanced by ADX and suppressed by corticosterone. These results suggest that suppression of LH pulsatility by stress is mediated by PGs in the brain, and that increased release of endogenous glucocorticoids in response to stress counteracts this suppression by inhibiting PG synthesis, and thereby maintains reproductive function regardless of the nature of the stressor.
authors.affiliation: Department of Veterinary Physiology, Veterinary Medical Science, University of Tokyo, Tokyo 113-8657, Japan.
authors.forename: Takashi
authors.initials: T
authors.lastname: Matsuwaki
authors.forename: Yuko
authors.initials: Y
authors.lastname: Kayasuga
authors.forename: Keitaro
authors.initials: K
authors.lastname: Yamanouchi
authors.forename: Masugi
authors.initials: M
authors.lastname: Nishihara
mesh_terms: D000311:Adrenal Glands / Q000378:metabolism; D000818:Animals; D001831:Body Temperature; D001921:Brain / Q000378:metabolism*; D003345:Corticosterone / Q000097:blood / Q000494:pharmacology; D051546:Cyclooxygenase 2 / Q000378:metabolism; D003847:Deoxyglucose / Q000494:pharmacology; D005260:Female; D005938:Glucocorticoids / Q000378:metabolism*; D006062:Gonadotropins / Q000378:metabolism*; D007003:Hypoglycemia / Q000473:pathology; D007150:Immunohistochemistry; D007213:Indomethacin / Q000494:pharmacology; D007239:Infections / Q000473:pathology*; D008070:Lipopolysaccharides / Q000378:metabolism; D007986:Luteinizing Hormone / Q000378:metabolism; D011453:Prostaglandins / Q000378:metabolism*; D011863:Radioimmunoassay; D051381:Rats; D017208:Rats, Wistar; D012098:Reproduction; D012149:Restraint, Physical; D013997:Time Factors
chemical_list: D005938:Glucocorticoids; D006062:Gonadotropins; D008070:Lipopolysaccharides; D011453:Prostaglandins; D007986:Luteinizing Hormone; D003847:Deoxyglucose; D051546:Cyclooxygenase 2; D003345:Corticosterone; D007213:Indomethacin