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Cortical consequences of elevated intraocular pressure in a primate model of glaucoma Lam, Dawn Yuen Sic
Glaucoma is a disease which affects the optic nerve. Its effects lead to debilitating visual deficits and there are no known cures. The primate model of glaucoma was developed so that investigators can study this disease. Research in glaucoma has examined the disease at the level of the eye and at the level of the lateral geniculate nucleus; however, few have looked at the consequence of this disease at the level of the visual cortex. This study looks at the effects of elevated intraocular pressure (IOP) over a period of seven months by examining the density of metabolic activity markers and neurochemical markers in primary visual cortex. Elevated IOP was induced by unilaterally lasering the trabecular meshwork of primates. Elevated IOP was monitored periodically over a period of two to seven months before the animals were sacrificed and the cortex processed histochemically for cytochrome oxidase (CO) and immunohistochemically for growth-associated protein 43 (GAP-43), synaptophysin (SYN), γ-aminobutyric acid receptor (GABAa receptor) and calcium-dependent protein kinase II α (CAMKIIα). CO density was found to be lower in deprived eye columns than in non-deprived eye columns suggesting that there was a decrease in metabolic activity in the eye subjected to elevated IOP. GAP-43, SYN and GABAa receptor densities were found to be greater in non-deprived eye columns than in deprived eye columns. In contrast, CAMKIIα protein densities were found to be greater in deprived eye columns than in non-deprived eye columns. When comparing the optical densities in the visual cortex of experimental animals to normal animals, the protein densities of GAP-43 and SYN were found to be higher in the experimental animals than in the normal animals. The protein densities of GABAa receptor and CAMKIIα were found to be lower in experimental animals than in normal animals. Our results suggest that elevated IOP caused cortical changes as early as two months post-elevated IOP. These changes continued through to seven months post-elevated IOP.
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