Fig. 1

Expression of Aif1 and Cd68 are attenuated in Bax-deficient mice after optic nerve crush. Wild-type and Bax ^−/− mice were subjected to crush injury and evaluated for microglial activation markers. a In wild-type mice, the mRNA expression of Aif1 peaked by 7 days post-injury, and then declined at 14 days and again at 21 days. In the Bax ^−/− mice, Aif1 expression was significantly attenuated relative to wild-type mice at 7 and 14 days. By 21 days, the levels of Aif1 appeared to be returning to baseline in both genotypes, and were no longer significantly different (P = 0.07). b The change in Cd68 expression followed a similar trend as Aif1, with levels peaking in the wild-type mice at 7 days before declining at 14 and again at 21 days. The Bax ^−/− mice, however, exhibited a significant attenuation in Cd68 expression at 7 and 14 days post-crush. By 21 days, expression in the knockout mice was significantly elevated over the wild types; however, expression in both genotypes remained low. Data is presented as mean ± SD. *P < 0.005. For each genotype at each time point, n ≥ 3