Regulation of testosterone secretion by prolactin in male rats

✍ Scribed by William J. Huang; Jiun-Yih Yeh; Shiow-Chwen Tsai; Ho Lin; Yu-Chung Chiao; Jiann-Jong Chen; Chien-Chen Lu; Seng-Wong Hwang; Shyi-Wu Wang; Luke S. Chang; Paulus S. Wang

• Publisher: John Wiley and Sons
• Year: 1999
• Tongue: English
• Weight: 128 KB
• Volume: 74
• Category: Article
• ISSN: 0730-2312
• DOI: 10.1002/(sici)1097-4644(19990701)74:1<111::aid-jcb12>3.0.co;2-i

✦ Synopsis

The goal of this study was to characterize the mechanism by which hyperprolactinemia alters testosterone production in rat testicular interstitial cells (TICs). Hyperprolactinemia was induced by grafting 2 anterior pituitary (AP) glands under the subcapsular space of the kidney in experimental rats. Control rats were grafted with brain cortex (CX). Six weeks post-grafting, rats were challenged with human chorionic gonadotropin (hCG) then, the changes in either plasma testosterone or luteinizing hormone was measured. Additionally, TICs were isolated and challenged in vitro with hCG or prolactin, and the testosterone release measured by radioimmunoassay. Further investigation in signal transduction as intracellular 3Ј:5Ј cyclic adenosine monophosphate (cAMP) production was observed under a regulation of forskolin or SQ22536. After the challenge of hCG or GnRH, the AP-grafted rats showed a suppressed response in testosterone release as compared to those in the CX-grafted group. The in vitro data from the AP-grafted rats compared to the CX-grafted animals showed a diminished response in testosterone release upon hCG stimulation. Administration of forskolin or SQ22536 disclosed dysfunction of adenylate cyclase in TICs from the AP-grafted rats. When 8-Br-cAMP was incubated with TICs, the testosterone production was lower in the AP-grafted compared to the CX-grafted group. These results suggest that in addition to adenylate cyclase dysfunction, inefficiency of post-cAMP pathways are also involved in the hypogonadism elicited by hyperprolactinemia in rats.