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Endocrinology, Vol 134, 158-163, Copyright © 1994 by Endocrine Society
ARTICLES |
JM McAndrews, SJ Ringstrom, KD Dahl and NB Schwartz
Department of Neurobiology and Physiology, Northwestern University, Evanston, Illinois 60208.
Experimental objectives were to determine: 1) if the native glucocorticoid, corticosterone (B), can selectively increase pituitary FSH and FSH beta messenger RNA (mRNA) in the presence or absence of a GnRH signal; and 2) if B affects the biological activity of the gonadotropins. Metestrous female rats were implanted with cholesterol or B. Each implant group received 100 micrograms GnRH antagonist or control injections every 48 h beginning at the time of implantation, and were killed 5 days later. B significantly increased bioactive serum FSH, with or without GnRH antagonist. GnRH antagonist decreased bioactive serum FSH. Immunoreactive serum FSH was not affected by any treatment. B did not affect bioactive serum LH, but GnRH antagonist significantly suppressed bioactive serum LH. Immunoreactive serum LH was significantly lowered by either B or GnRH antagonist. Neither bioactive nor immunoreactive pituitary FSH or LH content were affected by B, GnRH antagonist, or combined treatments, and no treatment affected alpha or LH beta mRNA. B significantly increased FSH beta mRNA specifically, in the presence or absence of GnRH antagonist. These results demonstrate that corticosterone can increase biological activity of secreted FSH and increase FSH beta mRNA in the absence of a GnRH signal, suggesting a direct effect on the anterior pituitary gland.
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