Reduction in Testicular Function in Rats

Abstract

Chronic administration of dexamethasone in drinking water to maternal rats from days 15 to 21 of gestation (1) reduced plasma testosterone concentrations in male fetuses between days 19 and 21 but not earlier on day 18 and abolished the prenatal peak of plasma testosterone which normally occurs on day 19 of gestation, and (2) suppressed the postnatal surge of plasma testosterone in male newborns 1.5 and 2 h after delivery at term by cesarean section. The administration of dexamethasone to male fetuses at birth induced 1 h later a slight but not significant increase in hypothalamic gonadotropin-releasing hormone (GnRH) and pituitary luteinizing hormone (LH) contents, reduced drastically plasma LH levels and completely prevented the postnatal surge of plasma testosterone which occurred normally in littermate controls. A rise in pituitary LH content, and a sharp reduction in plasma LH and testosterone concentrations were noted in 19-day-old male fetuses whose mothers were acutely treated with dexamethasone on day 18 of gestation. Similar evolutions for LH were observed in littermate females. These results suggest that the inhibitory effects of exogenous glucocorticoids on testosterone secretion could be mediated in both fetuses and newborns at least partially through suppression of the hypothalamic and pituitary secretion of GnRH and LH, respectively, and provide insight how stress or hormone imbalance may affect the development of this neuroendocrine system.

Blockage of N-Methyl-<i>D</i>-Aspartate Receptors Decreases Testosterone Levels and Enhances Postnatal Neuronal Apoptosis in the Preoptic Area of Male Rats

“…Our previous results indicated that the protein expression of NMDA receptor was higher in males than in females at both PND 1 and PND 3 [6]. In the present results, the protein expression of NMDA receptor is higher in male than in female fetuses at embryonic day 16, the day preceding the prenatal testosterone peak [3, 4]. Furthermore, serum levels of testosterone declined significantly on ED 18, when NMDA receptors were blocked by MK-801 the day before (fig.…”

“…In the prenatal period, testosterone levels are elevated only in male, not in female fetuses during embryonic days 17–19 [3, 4]. Moreover, testosterone has been reported to have profound inhibitory effects on the incidence of apoptosis in the sexually dimorphic nucleus of the preoptic area (SDN-POA) [5].…”

Maternal Dexamethasone Exposure Alters Synaptic Inputs to Gonadotropin-Releasing Hormone Neurons in the Early Postnatal Rat

“…Gestational stress alters the dendritic length and branching of neurons in the sexually dimorphic medial POA of adult males, suggesting possible modification of the neuronal activity and sexual behavior during adulthood (25). Exposure to the glucocorticoid receptor agonist, dexamethasone (DEX), during fetal stages reduce plasma testosterone levels, alter sexual maturation and reproductive behavior in male rat offpring (26–28), as well as delay pubertal onset with irregular estrous cycle in female rodent offspring (29, 30). Taken together, these changes are attributed to the effect of glucocorticoid exposure during fetal stages along the hypothalamic–pituitary–gonadal axis during development.…”

Maternal Dexamethasone Exposure Inhibits the Gonadotropin-Releasing Hormone Neuronal Movement in the Preoptic Area of Rat Offspring

“…Early-life DEX exposure has been shown to decrease the hypothalamic GnRH expression levels in both fetal and pubertal stages [28,29]. A subpopulation of GnRH neurons in rats and mice co-express the GC receptor [30,31], suggesting possible direct effect of excess GC on the GnRH neurons.…”