Fig. 11

Genetic ablation of Panx1 from RGCs does not reduce macroglial activation after optic nerve crush. We hypothesized that PANX1 hemichannels mediated ATP release from dying RGCs, and we examined the role of this protein in the crush paradigm by using mice genetically deficient for Panx1 in either RGCs or all cell types. a QPCR analysis showed that, relative to wild-type mice, total knockout mice expressed undetectable levels of Panx1, while RGC conditional knockout mice exhibited a 50 % reduction in mRNA expression. b Wild-type and Panx1-deficient mice were then subjected to crush and analyzed for macroglial activation. Wild-type mice exhibited characteristic Gfap expression, with levels peaking at 7 days before declining at 14 and 21 days. Similarly, at 7 days in the Panx1 ^−/− mice, Gfap mRNA abundance was highest, and gradually declined at 14 and 21 days. Mice deficient for Panx1 in RGCs exhibited sustained levels of macroglial activation as Gfap expression rose between 7 and 14 days, and remained significantly elevated above wild-type mice at 21 days post-crush. Data is presented as mean ± SD. *P < 0.0005, **P < 0.0001. For each genotype at each time point, n ≥ 3