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Abstract :
[en] Testosterone activates male sexual behavior partly through its conversion into 17β-estradiol (E2) by the enzyme aromatase in the preoptic area. The classical mechanism of action for E2 involves changes in gene transcription resulting in slow effects on behavior. In parallel, aromatase activity (AA) in the brain is also controlled by slow genomic mechanisms including mainly an increase in transcription following exposure to testosterone or its metabolites. However, rapid effects of E2 in the brain mediated by non-genomic mechanisms have also been documented. In parallel, it has recently been shown that AA can be rapidly modulated (within min) in vitro by changes in intracellular calcium concentration such as those produced by neurotransmitter action. These changes in enzymatic activity could result in rapid changes in the bioavailability of E2 obviously required to sustain rapid effects of this steroid. We investigated here the possible significance of the rapid modulations of AA in the control of male sexual behavior by quantifying the acute effects of single IP injections of E2 or VorozoleTM (VOR), a non-steroidal aromatase inhibitor, on male sexual behavior in quail. E2 (500µg/kg) injected 15 min before testing significantly stimulated copulatory behavior in castrated birds chronically treated with a low dose of T (2 mm long Silastic implant) unable by itself to elicit a complete copulatory sequence in most birds. VOR (30 mg/kg) significantly reduced copulation in gonadally intact males and in castrates treated with 40 mm T implants (CX+T40). Maximal effects were observed between 30 and 45 min after injection. VOR also inhibited appetitive sexual behavior measured by the rate of rhythmic cloacal sphincter movements in CX+T40 birds with a maximal effect at 30 min. Taken together, these data show that the rapid modulation of the availability of E2 in the brain rapidly affects male sexual behavior