Clinical Note

GnRH Deficiency

Persons who are deficient in GnRH fail to experience pubertal development and remain sexually juvenile. GnRH deficiency is treated with the aid of a pump that delivers GnRH under the skin in intermittent pulses every 2 hours. This regimen induces pubertal development and normal reproductive function. Treatment with a long-acting analog of GnRH that provides constant stimulation to the pituitary is ineffective in restoring normal function. Because treatment with a long-acting analog of GnRH desensitizes the pituitary gland and blocks gonadotropin secretion, this regimen has been used successfully to arrest premature sexual development in children suffering from precocious puberty.

mobilization of intracellular calcium and activation of protein kinase C. Transcription of genes for FSHp, LHp, and the common a subunit depends upon increased cytosolic calcium and several protein kinases for which the activation pathways are not understood. Secretion of gonadotropins depends upon the increase in intracellular calcium achieved by mobilizing calcium from intracellu-lar stores and by activating membrane calcium channels. Desensitization of gonadotropes after prolonged uninterrupted exposure to GnRH appears to result from the combined effects of downregulation of GnRH receptors, downregulation of calcium channels associated with secretion, and a decrease in the releasable storage pool of gonadotropin.

Negative Feedback Regulators

The hormones FSH and LH originate in the same pituitary cell whose secretory activity is stimulated by the same hypothalamic hormone, GnRH. Nevertheless, secretion of FSH is controlled independently of LH secretion by negative feedback signals that relate to the separate functions of the two gonadotropins. Although castration is followed by increased secretion of both FSH and LH, only LH is restored to normal when physiological amounts of testosterone are given. Failure of testicular descent into the scrotum (cryptorchidism) may result in destruction of the germinal epithelium without affecting Leydig cells. With this condition, blood levels of testosterone and LH are normal, but FSH is elevated. Thus, testosterone, which is secreted in response to LH, acts as a feedback regulator of LH and hence of its own secretion. By this reasoning, we would expect that spermatogenesis, which is stimulated by FSH, might be associated with secretion of a substance that reflects gamete production. Indeed, FSH stimulates the Sertoli cells to synthesize and secrete a glycoprotein called inhibin, which acts as a feedback inhibitor of FSH.

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