Formation of behaviorally effective 17 beta-estradiol in the dove brain: steroid control of preoptic aromatase.

The preoptic area (POA) of the male dove is a known target area for separable behavioral actions of testosterone and 17 beta-estradiol (E2) and contains an active aromatase system. We have examined the regulatory influence of gonadal hormones on aromatase using an in vitro microassay that measures conversion of [1 alpha, 2 alpha-3H]testosterone to E2 in anatomically defined brain samples of individual animals. Preoptic aromatase activity, which is higher in males than females, is decreased (77%) in both short (30 day) and long term (180 day) castrates, indicating that gonadal hormones maintain POA aromatase activity. Basal levels of POA activity are not influenced by the period of hormonal deficit. Low levels of aromatase activity detected in area basalis are also unaffected by castration. Intramuscular testosterone propionate rapidly increases aromatase activity (within 12 h) specifically in POA of castrated males. The inductive effect of testosterone propionate in castrated doves is not increased by limited behavioral interactions in a test situation with sexually active females. A nonaromatizable androgen, 5 alpha-dihydrotestosterone, has no effect on POA aromatase activity, whereas the activity of this enzyme is restored to levels of sexually active males by systemic E2. Diethylstilbestrol has a similar, though less potent effect, indicating an estrogenic action on the enzyme. We conclude that circulating androgen modulates preoptic aromatase activity. The product of the reaction, E2, is also likely to be involved as part of a positive feedback system.