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The Regulation of Gonadotropin-Releasing Hormone-Induced Calcium Signals in Male Rat Gonadotrophs by Testosterone Is Mediated by Dihydrotestosterone¹

Department of Physiology, Monash University, Clayton, Victoria 3168, Australia

Address all correspondence and requests for reprints to: Dr. B. J. Canny, Department of Physiology, Monash University, Clayton, Victoria 3168, Australia. E-mail: ben.canny{at}med.monash.edu.au

The biological effects of testosterone (T) may be mediated directly by T or indirectly by its metabolites, dihydrotestosterone (DHT) and estradiol. The present study examined whether the metabolism of T is involved in the regulation of GnRH-induced Ca²⁺ signaling at the pituitary. In gonadotrophs from castrated rats, a significantly greater percentage of gonadotrophs demonstrated oscillatory Ca²⁺ responses to 100 nM GnRH than cells from intact rats (72% vs. 24%; P < 0.05). This increase was prevented by the administration of T propionate (0.1 mg/kg·day), DHT benzoate (2 mg/kg·day,), estradiol benzoate (EB; 5 µg/kg·day), or the combination of the above doses of DHT benzoate and EB. In all cases the proportion of gonadotrophs from the steroid-treated rats having oscillatory Ca²⁺ responses to 100 nM GnRH was between 21–25% (P > 0.05, compared with intact rats). To assess the importance of T metabolism, intact male rats were treated with the aromatase inhibitor letrozole (1 mg/kg·day), the 5-reductase inhibitor finasteride (50 mg/kg·day), or their respective vehicles for 7 days. Letrozole had no effect on GnRH-induced Ca²⁺ signals, serum LH concentrations, or ventral prostate or testes weight. Finasteride treatment, however, mimicked the effects of castration, with significantly more gonadotrophs exhibiting Ca²⁺ oscillations in response to 100 nM GnRH than gonadotrophs from the vehicle-treated group (71% vs. 20% respectively; P < 0.05). Finasteride also caused a significant (P < 0.05) decrease in prostatic weight and DHT concentration, but had no significant effect on either prostatic T or serum LH concentrations. These findings suggest that in the intact male rat, the effects of T on GnRH-induced Ca²⁺ signaling are preferentially mediated via DHT. The results of this study also show that in the absence of androgens, estradiol may regulate GnRH-induced Ca²⁺ signaling in the male rat pituitary.

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