Axotomy induces cytochrome c release in retinal ganglion cells.

Activation of caspase-3 and -9 has been implicated in the death of axotomized retinal ganglion cells (RGCs). The upstream pathways involved in the activation of these caspases, however, remain unknown. The aim of the current study is to examine the role of cytochrome c release in axotomized RGC death using immuno-histochemistry. We found that while only a low level of cytochrome c immunoreactivity was evident in normal retina, cytochrome c immunoreactivity increased markedly at 1 day post-axotomy, peaked at 3 days post-axotomy, and decreased thereafter. In addition, cytochrome c immunoreactivity localized almost exclusively to RGCs, suggesting that the cytochrome c release observed was injury-related. Our data indicate that cytochrome c release potentially contributes to the death of axotomized RGCs.