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Mechanism of hormonally induced refractoriness of ovarian adenylate cyclase to luteinizing hormone and prostaglandin E.
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1977
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GynecologyOvarian Adenylate CyclaseReproductive BiologyCellular PhysiologyOvarian AgingOvarian CancerPituitary GlandPublic HealthProstaglandin EActinomycin DBiochemistryEndocrine MechanismHormonal ReceptorInduced RefractorinessRat Graafian FolliclesCyclic AmpEndocrinologyCell BiologyOvarian HormoneProtein PhosphorylationSignal TransductionUterine ReceptivityPhysiologyMedicineReproductive Hormone
Stimulation by prostaglandinE2 (PGE2) or luteinizing hormone (LH) of cyclic AMP (cAMP) production by rat Graafian follicles was reduced when the follicles were cultured for 3-6 hours in PGE2 or 12-24 hours in cAMP. The follicles regained adenylcyclase response to PGE2 when held in a PG-free medium, but refractoriness to LH remained even after culture without LH for 8 hours or in anti-LH antiserum. Follicle desensitization to LH was not associated by a decrease in total number of LH-binding sites, nor by an altered activity of cAMP phosphodiesterase. Desensitized follicles responded fully to NaF, quanosine triphosphate (GTP), or guanylimidodiphosphate (Gpp(NH)p). Actinomycin D or cycloheximide prevented the development of refractoriness to PGE2 when added with PGE2. Actinomycin D also prevented desentization to LH. Therefore desensitization may involve synthesis of a protein that couples hormone reception to adenyl cyclase.