MECHANISM OF THE STRESS-INDUCED ATTENUATION OF THE TESTICULAR RESPONSE TO GONADOTROPIN - POSSIBLE INVOLVEMENT OF TESTICULAR OPIOIDS, A PERTUSSIS-TOXIN-SENSITIVE G-PROTEIN, AND PHOSPHODIESTERASE

This study examined the potential role of testicular opioids, a pertus sis toxin (PT)-sensitive G-protein, and phosphodiesterase in mediating the inhibitory effect of immobilization stress on testicular steroido genesis in adult rats. The experiments were initiated with enriched pr eparations of Leydig cells, but the stress effect was not sustained in vitro either as a result of the disruption of the morphology of the t estis and/or the time required for Leydig cell isolation. Consequently , testicular fragments from control and stressed (3-hour immobilizatio n) rats were used in these experiments. When fragments from stressed r ats were incubated for 2 hours in the absence and presence of human ch orionic gonadotropin (hCG) (0.1, 1, or 10 mIU), testosterone (T) produ ction in response to 1 and 10 mIU hCG was lower (P < 0.05 and 0.01, re spectively) than that from control fragments. Basal T secretion did no t differ between stressed and control fragments. Naloxone (1, 10, or 1 00 mu M), did not alter basal or hCG-stimulated T secretion from contr ol fragments, but it normalized the T response to hCG from stressed fr agments. Control fragments also showed a reduced T response (P < 0.05) to hCG in the presence of beta-endorphin (beta-E; 36 nM). Incubation of control fragments with PT (30 ng) did not alter basal or hCG-stimul ated T production. However, PT normalized (P < 0.01) hCG-stimulated T secretion from stressed fragments. Methylisobutylxanthine (MIX; 0.125 mM) elevated (P < 0.01) hCG-stimulated T production from control fragm ents, but hCG-stimulated T secretion from stressed fragments remained subnormal in the presence of the phosphodiesterase inhibitor. The data suggest that acute immobilization stress inhibits gonadotropin-induce d T production in adult male rats via a mechanism involving testicular opioids and a PT-sensitive G-protein. We found no evidence to suggest that a stress-induced increase in the activity of phosphodiesterase w as involved in this mechanism.