Ontogenic development of the responsiveness in cAMP synthesis to LH and PGE1 and gonadotropin receptors in the rat ovary.
Incubation of ovaries derived from rats aged 9, 13, 16, and 20 days with LH resulted in a significant rise in cAMP synthesis. The ovaries from 2- and 5-day-old rats were, however, unresponsive to stimulation by LH. By contrast, prostaglandin E1 (PGE1) evoked a sharp response in ovarian synthesis of cAMP even in 2-day-old rats. In order to determine why neonatal ovaries do not respond to LH, gonadotropic receptors have been studied. HCG binding sites were present in homogenates of untreated and gonadotropins primed rat ovaries. The specificity of this 125I-HCG binding was demonstrated by the competition of unlabeled HCG and LH for binding sites and failure of such binding to occur in specimens obtained from control tissues. FSH, ACTH and growth hormone were not able to compete significantly for 125I-HCG binding. The HCG receptor is present in ovaries during the whole postnatal period. The results suggest that the unresponsiveness of neonatal rat ovaries to LH is not caused by later maturation of gonadotropic receptors.
D000818:Animals; D006063:Chorionic Gonadotropin / Q000378:metabolism*; D000242:Cyclic AMP / Q000096:biosynthesis*; D005260:Female; D007986:Luteinizing Hormone / Q000494:pharmacology*; D010053:Ovary / Q000378:metabolism*; D011247:Pregnancy; D011458:Prostaglandins E / Q000494:pharmacology*; D051381:Rats; D011956:Receptors, Cell Surface / Q000187:drug effects
D006063:Chorionic Gonadotropin; D011458:Prostaglandins E; D011956:Receptors, Cell Surface; D007986:Luteinizing Hormone; D000242:Cyclic AMP