Molecular Mechanism of Gonadotropin Releasing Hormone Action. II. The Effector System*

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Abstract
I. Introduction GONADOTROPIN-releasing hormone (GnRH)1 is a decapeptide which is synthesized and stored in neurosecretory cells of the medial basal hypothalamus. The releasing hormone is released in a pulsatile manner into the hypophysial portal circulation and is transported to the anterior pituitary; here it regulates the secretion of the gonadotropins, LH and FSH, into the systemic circulation. Thus, GnRH is a humoral link between the neural and endocrine components of reproductive function (1). The preceding article dealt with the initial interaction of GnRH with the plasma membrane receptor for the releasing hormone. In this article the means by which occupancy of the receptor by an agonist is transduced into cellular responses is reviewed. II. Calcium-Dependent Actions of GnRH GnRH is one of a family of hormones and neurotransmitters which require Ca2+ for their biological actions. The observation that omission or chelation of Ca2+ in the extracellular medium blocks depolarization- or hypothalamic extract-stimulated LH release from pituitary tissue (2) provided an early indication of the importance of Ca2+, and subsequently the role of Ca2+ in this aspect of GnRH action has been evaluated systematically (3, 4). Agents which increase intracellular Ca2+ concentrations, such as ionophores, KC1 (by depolarization), or calcium-loaded liposomes, release LH with efficacies similar to that of GnRH; other physiological cations (Na2, Mg2+) cannot substitute for calcium in this activity (5).

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