Effects of Prenatal Stress on Reproductive Function in Male Rats

Glucocorticoid hormones suppress testosterone production by Leydig cells, by interacting with glucocorticoid receptors located in these steroid-producing cells. In adult prenatally stressed males, increases in blood corticosterone were found to be accompanied by increased testosterone levels, which may be due to a decrease in the number of glucose receptors in Leydig cells. The present study sought to test this hypothesis. Glucocorticoid receptor levels in Leydig cells were estimated by quantitative immunohistochemistry. We also studied measures of spermatogenesis and sperm quality, as well as reproductive potential, which was analyzed in terms of the ability of males to fertilize females and produce offspring. These studies demonstrated decreases in the number of spermatogenic cells in the spermatogenic epithelium of the seminiferous tubules of prenatally stressed males, despite the increased blood testosterone level. Morphometric indicators of the seminiferous tubules, such as the thickness and area of the spermatogenic epithelium, in prenatally stressed males were increased, as were the number and area of Sertoli cells. We found statistically significant increases in the numbers of anomalous and immobile spermatozoids isolated from the epididymis of prenatally stressed males. The number of Leydig cells in the interstitial tissue of the testes of these males was reduced, though their area increased as compared with control males. Glucocorticoid receptor levels in Leydig cells were decreased in prenatally stressed males. Nonetheless, these changes did not influence the ability of prenatally stressed males to fertilize females and produce offspring. These results lead to the conclusion that increased blood testosterone levels in prenatally stressed males on the background of elevated glucocorticoid hormones lead to reductions in the sensitivity of Leydig cells to glucocorticoids.