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Cellular aspects of the inhibitory actions of LH-RH on the ovary and testis.

It is now firmly established that LH-RH and its agonists can have direct inhibitory effects on gonadal function in male and female animals. The initial reaction to such findings was one of incredulity because they challenged one of the accepted 'truths' of endocrinology, namely that LH-RH was secreted only by hypothalamic neurones and acted only on the anterior pituitary. However, LH-RH, like other hypothalamic peptides (e.g. thyrotrophin-releasing hormone, somatostatin), is quite widely distributed throughout the body. Current evidence suggests that LH-RH-like peptides occur in spinal ganglia in the frog (Jan, Jan & Kuffler, 1979; Jan, Jan & Brownfield, 1980) and, in mammals, in the pineal gland (Wheaton, 1980), pancreas (Seppala, Wahlstrom & Leppaluoto, 1979; Wahlstrom & Seppala, 1979; Seppala & Wahlstrom, 1980a), certain human mammary tumours (Seppala & Wahlstrom, 1980b), the placenta (e.g. Khodr & Siler-Khodr, 1980; Lee, Seppala & Chard, 1981), ovary (Ying, Ling, Bohlen & Guillemin, 1981) and testis (Sharpe, Fraser, Cooper & Rommerts, 1981, 1982). In most of these instances the information available is restricted simply to a demonstration of the presence of LHRH-like activity, but there is already considerable evidence as to the nature, function and mode of action of the locally produced peptide in the ovary and testis. As most of this information has been derived from the observed effects of LH-RH or its agonists when injected into rats, it is appropriate to begin by reviewing this evidence. When LH-RH and its agonists are injected into intact or hypophysectomized male and female rats, the resultant inhibitory effects on gonadal function are strikingly similar. However, injection of large doses ofLH and hCG also results in similar inhibitory changes. Therefore, in intact rats injected with LH-RH agonists it is difficult to distinguish whether the observed changes reflect direct gonadal effects of the injected peptide or whether they are secondary to release of pituitary LH and perhaps FSH (for references and discussion see Labrie et al, 1980; Sharpe, 1980a). To avoid confusion this review will deal only with the reported gonadal effects of LH-RH and its agonists in vitro or in hypophysectomized animals. It is assumed that the results obtained under such conditions reflect in general the direct gonadal actions of LH-RH in the intact animal. It should also be remembered that most of the studies discussed below have used agonistic LH-RH analogues (LH-RH agonists) rather than LH-RH itself. However, when both have been studied the effects have been identical except that 10to 100-fold higher doses of LH-RH are required to produce effects comparable to those obtained using LH-RH agonists with substitutions at positions 6 and 10. This difference in potency is almost certainly a reflection of the greater susceptibility of LH-RH to enzymic breakdown (see Clayton & Catt, 1981). For purposes of simplicity, the term LH-RH rather than LH-RH agonist(s) is subsequently used throughout this review, but the two terms are considered to be inter-changeable.