Optometry and Vision Sciences - Theses
Permanent URI for this collection
Search Results
1 - 2 of 2
-
ItemTime course of retinal changes in models of chronic IOP elevation( 2010)Glaucoma is an increasingly common sight threatening disease. Our understanding of the pathogenesis requires good models for disease risk factors. This thesis refines models of chronic intraocular pressure elevation in rats. Non-invasive assessment showed evidence of widespread retinal dysfunction. It is clear that dysfunction was not solely determined by intraocular pressure, but is associated with either ocular trauma or agent toxicity. Clear methodological recommendations are provided to minimise widespread damage and thus provide improved models for understanding glaucoma.
-
ItemThe non-neural contributions to the pigmented rat ERG( 2009)Introduction: The aim of this study is to consider the contribution of the RPE and Müller cells to the pigmented rat ERG. Materials and Methods: Groups of Long-Evans pigmented rats (n = 4 to 9) were anesthetized (Ketamine and Xylazine) and treated in one eye with different combinations of pharmacological agents. Intravitreal injection of BaCl2, APB and PDA, as well as intravenous injection of sodium iodate were administered in vivo, in order to isolate the specific contribution of each cell populations. Long flashes (2.5 s) were generated by LEDs in a full field Ganzfeld bowl, and ERG recordings were sampled at a rate of 2.5 Hz at 15 levels of luminance. The effect of each of the treatments was analyzed in comparison to a vehicle control group (n = 7), and between each drug treatment, using a two-way ANOVA with a Bonferroni post-hoc test to consider the intensities levels at which significant effects were noted. Results: Inhibition of Müller cells with BaCl2 treatment caused a b-wave enhancement attributable in part to the loss of the slow PIII. However, the slow PIII loss could not completely account for the enhancement. In addition, BaCl2 also alters what seems to be a bipolar cell driven PII enhancement, and induced an additional positive component on the ascending limb of the b-wave. A reduction of the c-wave could also be attributed to the loss of the slow PIII. The slow PIII exhibits an overshoot and a relative positivity after 1 s. Inhibition of RPE cells with sodium iodate caused a larger trough following the b-wave, attributed to the loss of the positive PI, but not a c-wave reduction. Conclusions: Pigmented rats exhibit a unique component structure where Müller cell slow PIII is the generator of the c-wave, while the RPE contributes a small PI component which peaks at the c-trough just following the b-wave.