ESTROGEN PROMOTES NEURON ADDITION TO AN AVIAN SONG-CONTROL NUCLEUS BYREGULATING POSTMITOTIC EVENTS

Only male zebra finches sing and several telencephalic song control re gions exhibit sex differences in neuron number that presumably reflect effects of estrogen (E2) exerted during the first few posthatch weeks . That is, implanting females with E2 during this time masculinizes ne uron number and instills the capacity for vocal behavior. In certain s ong regions, E2 masculinizes neuron number by preventing the naturally -occurring death of neurons, long after their production, migration an d process outgrowth are complete. However, in the Higher Vocal Center (HVC), the cellular mechanisms by which E2 establishes sex differences in neuron number are poorly understood. In contrast with other song r egions, HVC neurogenesis overlaps with sexual differentiation and the incorporation of new neurons is greater in young males and E2-treated females, than in normal females. However, it is not known whether E2 p romotes the addition of HVC neurons by stimulating their production, s pecification, and/or survival. To address this issue we injected males and females with [H-3]thymidine on days 15 and 16 to label a small gr oup of sexually dimorphic HVC neuronal cohorts born during sexual diff erentiation. Afterwards, on day 17, females were implanted with Silast ic pellets filled with estradiol benzoate (EB) or left empty. We repor t here that EB exposure on day 17 masculinized (increased) the number of neurons in the HVC at day 35 that were labeled by [3H]thymidine inj ections on days 15/16. Thus, EB was able to increase cell number among at least some HVC neuronal cohorts after their final division, implyi ng estrogenic regulation of post-mitotic events. When viewed with othe r studies that have examined the development of sex differences in the HVC, our results suggest that during sexual differentiation E2 promot es the specification and/or early survival of HVC neurons.