Abstract
Accumulating evidence supports an active role of non-neuronal cells in retinal ganglion cell (RGC) degeneration in glaucoma. Microglia are the resident immune surveillance cells of the CNS, are exquisitely sensitive to tissue stress and injury, and have been implicated in multiple neurodegenerative diseases, including glaucoma. Activated microglia converge on the initial site of axonal injury in human glaucoma, yet, their part in glaucoma pathophysiology remains unclear. In particular, it is unclear whether microglia activation precedes or is a late consequence of retinal ganglion cell (RGC) decline.
To address this we characterized the spatio-temporal distribution and activation of microglia in the retina and optic nerve head of DBA/2J (D2) mice, which model chronic glaucoma. These mice undergo iris atrophy leading to pigment dispersion, IOP elevation and an age-related, progressive decline in RGCs (Libby et al., 2005). In the D2 retina there has been no detailed analysis of microglial changes with age and