Human Reproduction, Vol. 9, No. 12, pp. 2247-2254, 1994
© 1994 European Society of Human Reproduction and Embryology
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Endocrinology: Stimulation of ovarian adenylyl cyclase activity by gonadotrophins during the natural and gonadotrophin-induced cycles in the hamster
Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, University of California, Irvine, 101 The City Drive Orange, CA 92668, USA
Correspondence: 2To whom correspondence should be addressed
In this study we utilized the hamster ovary as a model to investigate the effects of ovulation induction with gonadotrophin on the activation of the signal transducer effector system, adenylyl cyclase (AC). For this purpose, we prepared membrane particles from the ovary and analysed both gonadotrophin-sensitive AC and non-receptor-mediated activation during a cycle in which ovulation and luteinization were achieved by pregnant mare’s serum gonadotrophin (PMSG)/human chorionic gonadotrophin (HCG) administration. Results were directly compared with AC activation in similarly prepared membranes obtained at different stages of the natural unstimulated cycle. AC activity was quantified by the direct conversion of ATP substrate into cyclic adenosine monophosphate (cAMP). Measurements of ovarian weights, serum oestradiol and progesterone concentrations provided a solid base from which to evaluate the functional status of the ovary at each time period during the natural and stimulated cycles. We found that ovarian membranes contain functional components of the AC system and demonstrated that AC is highly dependent on hormonal changes and the functional state of the ovary. Thus, during the natural cycle, ovarian AC showed relatively constant responsiveness to follicle-stimulating hormone (FSH) throughout the cycle, whereas responsiveness to luteinizing hormone (LH)/HCG reached its peak during the luteal phase. On the other hand, during the stimulated cycle, sensitivity to FSH and LH/HCG varied considerably, being absent during the peri-ovulatory period. AC responsiveness to gonadotrophins was only regained 48 h after ovulation. Also during the peri-ovulatory period of the gonadotrophin-induced cycle, stimulation of ovarian AC with non-hormonal activators declined. However, the rate of cAMP production in response to these activators remained very high, indicating that despite refractoriness to gonadotrophins, ovarian AC retained the capacity to generate cAMP at near maximal efficiency. Basal (non-stimulated) activity, guanine nucleotide activation, hormone responsiveness and stimulation by the non-hormonal activators NaF and forskolin were all significantly increased in comparison with the natural cycle. Basal activity alone was 
7-fold higher than the activity observed during the unstimulated cycle. These results suggest that subsequent to exogenous gonadotrophin administration, the transmembrane effector AC system must be primed for a higher level of activity in the ovarian tissue. This priming of the ovarian AC system by exogenous gonadotrophin was also evident when the enzyme was measured under conditions allowing maximal activity, i.e. in the presence of a combination of NaF and forskolin. Maximal AC activity increased 4- to 5-fold compared with the natural cycle. We conclude that gonadotrophin administration inducing ovulation causes profound alterations in the expression of AC in ovarian membranes. Gonadotrophin treatment increased the enzyme activity and induced a temporal desensitization to FSH and LH/HCG in the peri-ovulatory period of the stimulated cycle. Because the gonadotrophin-sensitive AC system represents the capacity of FSH and LH/HCG receptors to couple and elicit a biological response, our results provide new insights into the cellular mechanisms that regulate ovarian activity during induction of ovulation.
Key words: adenylyl cyclase/gonadotrophins/natural cycle/ovarian function/ovulation induction
1Present address: Reproductive Technology Laboratories, 1245 16th Street, Suite 105, Santa Monica, CA 90404, USA
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