Regulation of testicular LH receptors by homologous hormone: in vitro studies on receptor occupancy and receptor loss.

A method is described which makes use of 4M MgCl, to dissociate the testicular luteinizing hormone-receptor complex without altering either the binding capacity or binding affinity of the receptor. Using this method, it was demonstrated that in vitro incubation at 4" of decapsulated rat testes with various concentratznmuteinizing hormone or with human chorionic gonadotropin resulted in a reduction in binding capacity. This reduction of binding capacity could not be completely accounted for by occupation of receptors by homologous hormone, suggesting that receptors were lost. Thus negative regulation of LH receptors by LH and hCG was observed. The reduction in LH binding capacity was specific for LH and hCG, dose dependent and time related. FSH, prolactin and growth hormone did not exert the same effect. LH* or hCG* initiates its action in the testis by binding to specific membrane receptors of Leydig cells. Although it has been reported that less than 1 per cent occupation of these receptors is necessary to elicit a maximum response in testosterone production (testicular responsiveness), it is not known whether the non-occupied receptors are really "spare" and nonessential. We recently demonstrated that hypophysectomy of adult male rats leads to an 85% reduction of available testicular LH receptor sites and a 60% reduction in testicular responsiveness six days following surgery (1). If LH administration is initiated at the time of hypophysectomy and continued twice daily for six days, testicular responsiveness is maintained at normal or above normal levels, while available LH receptor sites are even lower than in the hypophysectomized saline injected control animals (1). These studies suggest that maximal responsiveness can be elicited with relatively few receptors. To determine whether the apparent low levels of *Abbreviations: Luteinizing hormone, LH; human chorionic gonadotropin, hCG; follicle stimulating hormone, FSH.