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  • Title: Electroretinogram and visual-evoked potential assessment of retinal and central visual function in a rat ocular hypertension model of glaucoma.
    Author: Georgiou AL, Guo L, Francesca Cordeiro M, Salt TE.
    Journal: Curr Eye Res; 2014 May; 39(5):472-86. PubMed ID: 24215221.
    Abstract:
    PURPOSE/AIM: The aim of the study was to investigate the long-term functional changes that may occur in the retina and visual cortex in a rat ocular hypertension (OHT) model of glaucoma, used in our lab for treatment studies, using electroretinogram (ERG) and visual-evoked potential (VEP) cortical recordings in order to test the hypothesis that experimental glaucoma has differential retinal and central effects. MATERIALS AND METHODS: Experimental glaucoma was induced unilaterally in Dark Agouti rats using hypertonic saline injection into the episcleral veins. After 3, 8, 16 and 26 weeks, ERGs and VEPs were recorded under scotopic conditions using brief full-field white flashes (10 μcd s m(-2) to 10.4 cd s m(-2)) and under photopic conditions using a rod-adapting background and white light flashes (0.13-10.4 cd s m(-2)). RESULTS: At 16 and 26 weeks after OHT induction, there was a significant reduction in the amplitudes of the a- (50% and 30% of unoperated eye values, respectively) and b-waves (55% and 40%, respectively) of the scotopic ERG and the b-waves of the photopic ERG (55% and 45%, respectively) in the glaucomatous eyes. However, no significant changes in the VEPs simultaneously recorded over the visual cortex were seen at any of the time points. CONCLUSIONS: The reductions in ERG amplitudes suggest that this model of glaucoma not only causes retinal ganglion cell (RGC) degeneration but also degeneration of the outer retinal cells, and this was confirmed by histology showing a reduction in the outer retinal layers in the glaucomatous eyes. Cortical VEPs did not show detrimental effects suggesting that the retinal damage in this model was not extensive enough to be detected with the VEP methods used or that there could be central compensation in this model of glaucoma.
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