Mechanisms regulating sexual differentiation of the zebra finch song system
present an intriguing puzzle. Masculine development of brain regions and b
ehavior can be induced in genetic females by posthatching estradiol treatme
nt. That result is consistent with the hypothesis that estradiol, converted
within the brain from testicular androgen via the aromatase enzyme, mascul
inizes neural structure and function. In contrast, treatment during specifi
c stages of development with the aromatase inhibitor Fadrozole has not prev
ented masculine development, and the presence of testicular tissue in genet
ic females did not induce masculine organization of neuroanatomy or singing
behavior. Fadrozole treatments in those previous studies were limited, how
ever, and most genetic females had both ovarian and testicular tissue. The
present experiments were designed to provide increased aromatase inhibition
and to reliably produce genetic females with only testicular tissue. Eggs
received a single injection at a later age or with higher doses of Fadrozol
e than had been used previously. Some embryos were exposed to Fadrozole mor
e frequently by either injecting eggs on 2 days of development or dipping t
hem for 10-12 days in Fadrozole. Finally, in some individuals from Fadrozol
e-treated eggs, the left gonad was removed, leaving each genetic male and f
emale with a single right testis. None of these treatments significantly af
fected development of the song system compared to appropriate control group
s. These results suggest that sexual differentiation of the zebra finch son
g system is not regulated by embryonic aromatase activity or by gonadal sec
retions and instead involves events that need not be mediated by steroid ho
rmones. (C) 1999 Academic Press.