Hormonal Regulation of Testicular Luteinizing Hormone and Prolactin Receptors

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Abstract
The effects of gonadotropic stimulation on testicular LH and PRL receptors were examined in the absence and presence of elevated serum PRL levels. In adult male rats, the administration of ovine LH (oLH) caused an increase in both PRL and LH receptors within 40–120 min. This initial rise in testicular receptors was followed by the transient loss and recovery of PRL sites and a more prolonged loss of LH receptors. In contrast, the administration of bovine PRL or the elevation of circulating PRL levels during metoclopramide infusion caused no change in the lactogenic sites. A significant positive effect of increased serum PRL levels on testicular LH receptors was observed during metoclopramide infusion, but this did not prevent the loss of LH receptors caused by the administration of oLH. Similarly, prior treatment with bovine PRL failed to prevent the LH-induced loss of testicular LH receptors. These findings demonstrate that PRL and LH receptors exhibit concomitant but distinct forms of regulation during Leydig cell stimulation by oLH. Testicular receptor sites for both LH and PRL undergo a common process of increased availability during the early phase of Leydig cell activation by gonadotropins. This transient increase in both binding sites is followed by a subsequent period of depletion that is short-lived for the PRL sites and prolonged for the LH receptors. The long term action of PRL on the maintenance of testicular LH receptors does not influence the acute increase and subsequent loss of sites that follows gonadotropic stimulation of the Leydig cells. (Endocrinology108: 1607, 1981)