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Gonadal Regulation of Hypothalamic Gonadotropin Releasing Hormone Release in Primates^*

Department of Physiology, University of Pittsburgh School of Medicine Pittsburgh, Pennsylvania 15261

Correspondence: Address requests for reprints to: Dr. Tony M. Plant, Department of Physiology, 614 Scaife Hall, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261.

Abstract

Introduction: THE DRIVE to the pituitary-gonadal axis originates within the central nervous system (CNS) and is transmitted to the gonadotropes of the adenohypophysis by an intermittent discharge of GnRH into the hypophysial portal circulation, an episodic pattern of hypothalamic neurosecretion that results in striking ultradian fluctuations in the concentration of this releasing factor in portal blood (1–3). In the rhesus monkey, as in nonprimate species (4), when the neurohumoral link between the brain and pituitary gland is interrupted, either by stalk section or by destruction of the arcuate nucleusmedian eminence region of the hypothalamus, pituitary gonadotropin secretion is essentially abolished and gonadal function arrested (5–9). Moreover, in monkeys with an intact hypophysial portal circulation, imraunoneutralization with anti-GnRH 7-globulins, or treatment with a GnRH antagonist, also results in a marked diminution in LH and FSH secretion (10–12). In the human female, a situation analogous to the hypothalamic lesioned monkey is observed in subjects with hypothalamic amenorrhea, as occurs for example in patients with Kailman's syndrome, in which the release of endogenous GnRH is abolished or severely compromised (13, 14).

Footnotes

^* The work from this laboratory, which is described in the review that follows, was supported by grants from the NIH (HD-08610 and HD-16851).

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