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SEVERAL aspects of the GnRH receptor and its signaling properties and secretory actions have been previously described (1–5). The characterization of GnRH receptors, their physiological regulation, and their relationship to reproductive function were discussed in 1981 (1). The role of Ca2+ as the second messenger, and of diacylglycerol (DAG) as a potential amplifier of the Ca2+ signaling in GnRHstimulated cells, was reviewed in 1986 (2). The molecular mechanism of GnRH action was further discussed in 1988, including the dependence of GnRH-induced secretion on phosphoinositide action (3, 4). Also, signal transduction in GnRH-stimulated cells was reviewed in 1990 as an example of a phospholipid-dependent pathway; the review addressed the interactions between cytoplasmic calcium and protein kinase C (PKC) in the control of gonadotropin synthesis and release, as well as the participation of phospholipase D (PLD), arachidonic acid (AA) and its metabolites in GnRHinduced signaling (5). Since 1990, there has been an explosive increase in information about GnRH receptors and their signaling properties.
Stojilković et al. (Mon,) studied this question.