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The DBA/2J mouse strain is an established model of spontaneous elevated IOP leading to retinal ganglion cell loss and optic disc ex-cavation first evident at approximately nine months of age. By age 18 months, advanced degeneration of the optic nerve is apparent. Saleh et al. (1239) measured pattern ERG (representing retinal ganglion cell (RGC) function) and flash ERG (representing outer retina function) responses from 64 DBA/2J mouse eyes over time (at one-month intervals) and demonstrated that PERG amplitude decreased to noise level in 50% of eyes at nine months of age (the approximate time of first evidence of optic disc excavation) and nearly 100% of eyes at 11 months. In the mean time, FERG amplitude was minimally affected. Change in PERG amplitude at two, 11 and 16 months was compared to change in RNFL thickness, measured histologically at these intervals, in independent groups of animals. The results suggest that by the time the PERG amplitude reaches noise levels (e.g., 11 months), RNFL thickness (and therefore axon counts) is decreased by only 40% compared to normal. Overall, loss of RNFL thickness lagged behind loss of PERG amplitude by approximately three months, or one-tenth of a mouse's lifespan. The authors fairly conclude that, in this model of glaucoma, RGCs undergo progressive dysfunction that precedes ganglion cell loss and suggest that neuroprotection studies using this model would benefit using a PERG endpoint as an early indicator of impending damage.