Regulation of Luteinizing-Hormone-Receptors and Steroidogenesis in the Neonatal Rat Testis

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Abstract
Testicular LH receptor regulation and steroidogenesis were studied in 5-day-old rats, in which Leydig cells are derived from the fetal population of interstitial cells. The affinity of hCG binding to the neonatal and adult testis was similar. The hCG-binding capacity per unit weight of tissue in the neonatal testis was 5–10% of the adult level but was very similar when expressed per Leydig cell. The sensitivity of the testosterone response to hCG was 4-fold higher in neonatal Leydig cells, whereas the basal and maximal rates of testosterone production were similar in neonatal and adult cells. No clear differences were seen in cAMP production. A low dose of hCG (20 IU/kg BW sc) induced in 1–3 days a 40–60% increase in LH receptors without affecting the Leydig cell number; such an effect was not observed in the adult. A higher dose of hCG (600 IU/kg BW sc) increased the number of Leydig cells per testis about 2-fold in 2 days, and a significant increase in testicular basal and hCGstimulated testosterone production occurred, in contrast to adult animals where similar treatment desensitized testosterone production. The high dose of hCG totally abolished available neonatal testis LH receptors, but complete recovery of binding occurred between 48 and 72 h. In contrast, more than 10 days were needed for complete recovery of LH receptors in adult testes. Measurements of tissue-bound hCG indicated that the decrease in neonatal testis LH binding was due to receptor occupancy without net loss of binding sites. Our results demonstrate that in comparison to the adult, the following features are characteristic of the fetal population of rat testis Leydig cells: 1) Testosterone production is more sensitive to gonadotropic stimulation. 2) No hCG-induced desensitization of androgen biosynthesis is seen. 3) Low dose hCG treatment increases the number of LH receptors. 4) High dose hCG treatment decreases LH binding for a shorter period than in the adult. The loss of binding is explained by receptor occupancy, without net loss of receptors. 5) High dose hCG treatment also causes a rapid increase in the number of Leydig cells.
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