Optometry and Vision Sciences - Research Publications

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Author: Vingrys, Algis × Author: Cole, Barry × Start date: 2011 × End date: 2014 ×

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    Effect of acute intraocular pressure challenge on rat retinal and cortical function
    Tsai, Tina I. ; Bui, Bang V. ; Vingrys, Algis J. (Association for Research in Vision and Ophthalmology (ARVO), 2014)
    Purpose: The global or gross response index of visual performance measured from the eye does not necessarily translate to global responses measured from the brain. A better understanding of this relationship would facilitate the monitoring of disease models that affect the visual pathway. We consider whether rod- and cone-retino-cortical-pathways are equally affected by acute IOP elevation. Methods: Acute, stepwise IOP elevation (10, 30, 40, 50, 60, 70 mm Hg) was induced in anesthetized dark- (N = 8) and light-adapted pigmented rats (N = 6). Electroretinogram (ERG) and visual evoked potentials (VEP) were simultaneously measured after 10 minutes at each step. Relative amplitudes (treated/baseline, %) as a function of IOP level were described with a cumulative normal function. Results: Our results showed decline in scotopic and photopic ERGs with IOP elevation. Photopic ERG responses were less sensitive to IOP challenge than scotopic ERG responses. Despite significant reductions of ganglion cell–mediated waveforms at 70 mm Hg, the VEP showed only subtle decreases in amplitude. Intraocular pressure elevation produced similar effects on rod- and cone-mediated VEP waveforms. Conclusions: We show that cone signals are less sensitive than rod ERGs to acute IOP challenge. Also, retinal signals are more sensitive than are cortical signals to IOP stress, suggesting that cortical processing may act to salvage reductions expected from attenuated retinal output.
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    Glial and neuronal dysfunction in streptozotocin-induced diabetic rats.
    Wong, VHY ; Vingrys, AJ ; Bui, BV (Springer Science and Business Media LLC, 2011-06)
    Neuronal dysfunction has been noted very soon after the induction of diabetes by streptozotocin injection in rats. It is not clear from anatomical evidence whether glial cell dysfunction accompanies the well-documented neuronal deficit. Here, we isolate the Müller cell driven slow-P3 component of the full-field electroretinogram and show that it is attenuated at 4 weeks following the onset of streptozotocin-hyperglycaemia. We also found a concurrent reduction in the sensitivity of the phototransduction cascade, as well as in the components of the electroretinogram known to indicate retinal ganglion cell and amacrine cell integrity. Our data support the idea that neuronal and Müller cell dysfunction occurs at the same time in streptozotocin-induced hyperglycaemia.