Control of gonadotropin secretion

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During the past year, numerous discoveries have been made regarding the control of gonadotropin secretion. Perhaps most important is the innate pulsatility of cloned hypothalamic gonadotropin-releasing hormone (GnRH)-secreting neuronal cell lines. This model and other data indicate that signalling via voltage-sensitive Ca2+ channels is integral to pulsatile GnRH release, and that GnRH secretion is enhanced by physiologic glucose concentrations, neuropeptide Y, and hypothalamic adrenergic β1 receptor stimulation. GnRH release is decreased by gamma aminobutyric acid receptor A, corticotropin-releasing hormone, and testosterone. At the pituitary level, GnRH pulse amplitude and frequency, testosterone, interleukin, corticotropin-releasing hormone, and progesterone modulate follicle stimulating hormone (FSH) and luteinizing hormone (LH) biosynthesis and secretion Studies in the monkey indicate that even arginine vasopressin may play an inhibitory role in controlling gonadotropin secretion. Importantly, GnRH, LH, FSH, and gonadal steroid secretion are developmentally regulated. In the male neonate, for example, a prominent surge of LH and testosterone occurs transiently. Changes in GnRH pulse frequency and amplitude control pituitary gonadotropin subunit gene expression, as well as glycoprotein hormone secretion. Steroid hormones appear to modulate both GnRH and LH and FSH secretion. In short, the hypothalamic-pituitary-gonadal axis is subject to exquisite multilevel regulation.

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