Abstract
Purpose: :
Light flickering at ~10 Hz induces dilation of retinal vessels, implying adaptation to increased metabolic demand. We tested the hypothesis that the PERG, a measure of retinal ganglion cell function, would be altered by superimposition of flicker in the mouse, and that PERG alteration would be relatively greater in DBA/2J mice prone to glaucoma with potentially altered baseline metabolism.
Methods: :
PERGs were recorded in 32 mice 2-3 months old (C57BL/6J, n=9; DBA/2J, n=10; DBA/2J.Gpnmb+, n=13) with superimposed flicker at either 10 Hz (test) or 100 Hz (control - beyond temporal resolution of mouse cone ERG). Flicker-induced PERG amplitude/latency changes were calculated as differences between test and control. PERG stimuli were horizontal gratings of 0.05 cycles/deg and 100% contrast. Flicker stimuli were bright white LED, and were asynchronous with the PERG stimulus, in order not to generate any recordable flicker ERG.
Results: :
Baseline PERG amplitudes were similar in the three strains. Superimposition of 10 Hz flicker induced increases of PERG latency in all strains (C57BL/6J, 15.4 ms (SE 2.7); DBA/2J, 22.3 ms (SE 3.8); DBA/2J.Gpnmb+, 5.9 ms (SE 3.1). Strain differences in latency were significant (ANOVA, P=0.006). Flicker-induced amplitude changes were unremarkable and not different among strains (ANOVA, P=0.25).
Conclusions: :
Previous studies in the rat have shown increased arterial blood flow and PO2 during flicker at ~10 Hz. Our results indicate that these metabolic changes are associated with increased PERG latency at constant PERG amplitude. PERG latency changes are relatively greater in pre-glaucomatous DBA/2J mice, possibly indicating altered neurovascular/neurometabolic response in a strain prone to glaucoma.
Keywords: ganglion cells • metabolism • electroretinography: non-clinical