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The present study was designed to test the effect of acute administration of dexamethasone on the postcastration and gonadotrophin-releasing hormone (GnRH)-induced rise of LH, and to examine whether the inhibitory action of glucocorticoids on LH secretion was mediated by the opioid system. Rats were castrated and injected 10–10·5 h later in a first set of experiments with saline, dexamethasone (250 µg/rat), nalmefene (2 mg/kg body weight) or nalmefene plus dexamethasone. The response to GnRH was tested 11 h after castration (time 0) in all groups. Dexamethasone caused a significant (P< 0·005) decrease in basal serum concentrations of LH, while saline and nalmefene did not induce any change. The administration of dexamethasone preceded by nalmefene increased basal concentrations of LH (1·6 times), with an effect significantly greater than that of dexamethasone (P< 0·001), nalmefene (P<0·05) or saline (P<0·005) alone. GnRH induced a significant (P < 0·001) increase in serum concentrations of LH in all groups. In a second set of experiments, administration of naloxone (2 mg/kg body weight) increased LH levels (P<0·05) and similarly reversed the inhibitory effect of dexamethasone on LH. These results indicate (1) that the inhibiting effect of dexamethasone on the post-castration rise of LH is likely to be exerted at a suprapituitary level, since dexamethasone does not decrease the GnRH stimulated LH response, (2) that opioid antagonists have the ability to reverse the glucocorticoid-inhibiting effect on LH and (3) that dexamethasone can enhance the effect of nalmefene at a time when serum concentrations of testosterone are at very low levels. We conclude, therefore, that dexamethasone regulates LH secretion, at least in part, through the same pathways as testosterone.

Journal of Endocrinology (1989) 121, 451–456