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K. Mohan, M. M. Harper, K. Schipull, A. Ghosh, A. G. Kanthasamy, A. Kanthasamy, R. H. Kardon, S. D. Grozdanic; Functional Retinal Ganglion Cell PERG Deficits in an Acute and Chronic Mouse Model of Parkinson’s Disease. Invest. Ophthalmol. Vis. Sci. 2010;51(13):5797.
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© ARVO (1962-2015); The Authors (2016-present)
To characterize the acute and chronic functional changes of the retina in a rodent model of Parkinson’s disease (PD) using pattern electroretinography (pERG).
Pattern evoked electroretinography was used to objectively measure retinal ganglion cell function. To elicit a pERG response, a black and white vertical stimuli was used (9° full field 1 Hz frequency, 1-30 Hz filter, 200 stimuli repetitions, photopic conditions). Baseline amplitudes (N35-P50 and P50-N95) and latencies (N35, P50, and N95) were evaluated in all mice prior to induction of PD (n=20). A PD phenotype was created by i.p. injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) acutely (5 injections in 1 day) or chronically (5 injections over 5 days) after evaluation of baseline pERG parameters.
Analysis of the acute MPTP model of PD revealed a significant decrease in the P50-N95 amplitude 1 day post induction (2.89±1.05 µV, mean±SEM) when compared to baseline recordings (8.02±1.18 µV; p=0.0151, Paired t-test). Analysis of P50-N95 amplitude in the chronic model of PD (0.89±0.48 µV p<0.05, ANOVA) revealed a significant decrease from baseline values at 16 days after induction of the model, however there were no significant deficits detected at 1, 4 and 8 days post induction. The pERG latencies were not significantly different from the pre-recorded values in both groups.
Acute and chronic models of PD show significant loss in retinal ganglion cell function as demonstrated by deficits in pERG amplitudes.
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