Calcium signaling and gonadotropin secretion
1Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Building 10, Rm. 8C407, Bethesda, MD 20892, USA.
Trends in Endocrinology and Metabolism: TEM
|September 1, 1989
Summary
Gonadotropin-releasing hormone (GnRH) triggers calcium release and luteinizing hormone (LH) release in pituitary cells. Calcium influx and protein kinase C are crucial for sustained hormone secretion and synthesis, while calcium channel inactivation causes desensitization.
Area of Science:
- Endocrinology
- Cell Signaling
- Reproductive Biology
Background:
- Pituitary gonadotrophs release luteinizing hormone (LH) upon stimulation by gonadotropin-releasing hormone (GnRH).
- GnRH triggers rapid intracellular calcium (InsP3-dependent) and sustained calcium influx, influencing LH release and synthesis.
Purpose of the Study:
- To elucidate the roles of calcium mobilization, influx, and protein kinase C in GnRH-stimulated gonadotropin secretion.
- To investigate the mechanisms underlying GnRH-induced desensitization of LH release.
Main Methods:
- Measurement of intracellular calcium levels and LH release in pituitary gonadotrophs.
- Analysis of the contribution of L-type and dihydropyridine-insensitive calcium channels.
- Assessment of protein kinase C involvement in hormone secretion and synthesis.
Main Results:
- GnRH induces biphasic calcium responses: initial InsP3-dependent peaks followed by sustained calcium influx.
- Receptor-mediated calcium entry via L-type and other channels sustains LH release and synthesis.
- Calcium-dependent inactivation of L-type channels contributes to the desensitization of gonadotropin secretion.
Conclusions:
- Sustained calcium influx and protein kinase C activity are essential for prolonged LH secretion and synthesis following GnRH stimulation.
- Calcium channel inactivation plays a key role in the desensitization process, limiting sustained gonadotropin release.
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