Abstract:
:In experiment I we studied the capacity of progesterone (P) and two nonsteroidal agents that activate lordosis, but do not bind to the progestin receptor (PR), i.e. luteinizing hormone-releasing hormone (LHRH) and prostaglandin E2 (PGE2) to induce sequential inhibition (SI) in ovariectomized estradiol-primed rats. The administration of 1 mg P, 5 micrograms LHRH or 100 micrograms PGE2 induced significant lordosis within 4 h. An injection of 1 mg P, 24 h after the administration of the above lordogenic agents, induced significant lordosis in rats pretreated with LHRH or PGE2, but not in those pretreated with P. Thus, only P induced SI (p < 0.025). In experiment II we investigated if progestin-induced SI results in a reduced capacity of the subjects to respond only to P or to other lordogenic agents. The synthetic progestin norgestrel (400 micrograms administered 24 h earlier) significantly reduced the responsiveness to P (p < 0.01), LHRH (p < 0.01), PGE2 (p < 0.025) and dibutyryl cyclic AMP (db cAMP p < 0.01). Results suggest that SI is triggered only by agents that bind to the PR (experiment I) and that it decreases the responsiveness of rats not only to P but also to other lordogenic agents (experiment II).
journal_name
Neuroendocrinologyjournal_title
Neuroendocrinologyauthors
González-Mariscal G,Melo AI,Beyer Cdoi
10.1159/000126457subject
Has Abstractpub_date
1993-05-01 00:00:00pages
940-5issue
5eissn
0028-3835issn
1423-0194journal_volume
57pub_type
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