Injury to the mammalian brain precedes a pronounced wave of secondary cellular degeneration (WSD). In mammals and birds, glial cells around injury increase the expression of the enzyme aromatase (estrogen-synthase) and locally produced estrogen decreases cellular degeneration. While several studies have documented a decrease in cellular degeneration at discrete time-points following brain damage, the role of upregulated glial aromatase on the dynamics of this WSD remains poorly described. In the present study, adult male zebra finches (Taeniopygia guttata) received injuries with a needle that contained the aromatase inhibitor fadrozole or vehicle into contralateral hemispheres. Birds were sacrificed 0, 2, 6, 24, 72hrs, 2 or 6 weeks post-injury. With the exception of the 0hr time-point (where no degeneration was detected), degeneration around vehicle-injury did not differ amongst all of the time-points evaluated post-vehicle insult. Degeneration around fadrozole-injury, however, peaked at 24-72hrs post-injury and decreased thereafter. Thus, the injury-induced WSD as described in mammals is detectable in zebra finches only following local aromatase inhibition. Aromatase expression was higher around fadrozole injury relative to saline injury up to 2 weeks post-insult, suggesting that aromatase inhibition dissipated sometime around 2 weeks post-injury. In the zebra finch, local estrogen synthesis by glial aromatase severely dampens the WSD following brain damage. Songbirds may be powerful models toward understanding the role of local estrogen synthesis on secondary brain damage.
Ryan Wynne is a Ph.D. graduate student majoring in biochemistry in the Department of Biological Sciences. Ryan earned his Bachelor’s degree in both chemistry and biochemistry from East Stroudsburg University in 2002. He is currently the president of the Biology Organization of Graduate Students and is the recipient of the Nemes Fellowship for the 2006-2007 academic year. Ryan’s research focuses on the roles the endocrine system plays in brain injury and repair.