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LH RECEPTORS AND STEROIDOGENESIS IN DISTINCT POPULATIONS OF LEYDIG CELLS *
Author(s) -
Payne Anita H.,
O'Shaughnessy Peter J.,
Chase David J.,
Dixon Gretchen E. K.,
Christensen A. Kent
Publication year - 1982
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1982.tb23168.x
Subject(s) - reproductive endocrinology , obstetrics and gynaecology , annals , reproductive medicine , medicine , reproductive biology , library science , biology , history , classics , hormone , pregnancy , lactation , computer science , genetics
Luteinizing hormone (LH) has been shown to be the only hormone essential for maintenance of testicular testosterone pr0duction.l LH mediates its effect on testicular steroidogenesis by binding to high affinity receptors in the plasma membrane of Leydig cells. In recent years, numerous investigators have reported that in vivo administration of LH or human chorionic gonadotropin (hCG) results in the reduction of the number of testicular LH receptors1-’ accompanied by a decrease in testosterone production 4, 6+ in response to subsequent stimulation by LH or hCG. Studies from our laboratory, however, have demonstrated that changes in LH receptor number may be dissociated from changes in LH-stimulated testosterone production following in vivo treatment with gonadotropins.1 We observed that only a single high dose of LH, 100 pg or greater, caused a decrease in testicular responsiveness, whereas twice daily injections of LH for six days or longer were accompanied by a time-related increase in in vivo testicular testosterone secretion in response to a subsequent stimulatory dose of LH. The LH-induced loss of testicular LH receptors was similar in rats that received a single high dose of LH and in rats that received twice daily injections. These observations indicate that different modes of in vivo LH treatment have markedly different effects on testicular responsiveness to subsequent LH/hCG stimulation. Interpretation of these results, however, is complicated by the possibility that chronic pituitary hormone treatment may change ( 1 ) sensitivity of the Leydig cells to subsequent LH stimulation, ( 2 ) secretion or clearance rate of testosterone, and/or ( 3 ) total number of Leydig cells. To distinguish among these possibilities, changes in Leydig cell LH receptor concentration and responsiveness to LH were assessed in the same cells after different modes of in vivo hormone treatment. Using Metrizamide gradient centrifugation to separate dispersed testicular cells, we found evidence for two distinct populations of Leydig cells.* Leydig cells of these two populations contain similar numbers of LH receptor sites but exhibit marked differences in testosterone production in response to in vitro