ACTIVATION OF SALMON GONADOTROPIN-RELEASING-HORMONE SYNTHESIS BY 17-ALPHA-METHYLTESTOSTERONE ADMINISTRATION IN YEARLING MASU SALMON, ONCORHYNCHUS-MASOU

Citation
M. Amano et al., ACTIVATION OF SALMON GONADOTROPIN-RELEASING-HORMONE SYNTHESIS BY 17-ALPHA-METHYLTESTOSTERONE ADMINISTRATION IN YEARLING MASU SALMON, ONCORHYNCHUS-MASOU, General and comparative endocrinology, 95(3), 1994, pp. 374-380
Citations number
17
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
00166480
Volume
95
Issue
3
Year of publication
1994
Pages
374 - 380
Database
ISI
SICI code
0016-6480(1994)95:3<374:AOSGSB>2.0.ZU;2-2
Abstract
Juvenile salmonid pituitary gonadotropin (GTH) contents are elevated a fter steroid hormone treatment, but the involvement of gonadotropin-re leasing hormone (GnRH) is unclear. Activation of salmon GnRH (sGnRH) s ynthesis by 17 alpha-methyltestosterone (MT) administration has been e xamined in the brain of yearling masu salmon (future precocious males and immature females) using an in situ hybridization technique combine d with radioimmunoassay. Oral MT application markedly increased pituit ary GTH II beta, but not GTH I beta, contents in both sexes. In future precocious males, MT treatment increased the number of cells expressi ng sGnRH mRNA in the preoptic area about threefold, whereas there were no significant differences in the olfactory bulbs and the ventral tel encephalon. No significant changes were observed in cell sizes nor the numbers of silver grain per 100 mu m(2) cell in any of the brain regi ons. Thus, in future precocious males, preoptic sGnRH neurons may be a ctivated by sex steroids. In contrast, no significant changes were obs erved in sGnRH mRNA levels of immature females after MT treatment. The se differences in responses to sex steroids of sGnRH cells in the preo ptic area between future precocious males and immature females suggest that MT has indirect actions via sGnRH and/or direct actions on the p ituitary in the former, and that MT acts directly on the pituitary in the latter. (C) 1994 Academic Press, Inc.