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Neurochemical Correlates of Cortical Plasticity after Unilateral Elevated Intraocular Pressure in a Primate Model of Glaucoma

¹From the Department of Ophthalmology and Visual Sciences, University of British Columbia, Vancouver, British Columbia, Canada; and the ²Department of Ophthalmology and Visual Sciences, University of Wisconsin, Madison, Wisconsin.

PURPOSE. To examine the time course of changes in the expression patterns of several synaptic plasticity markers in the primary visual cortex after unilateral elevated intraocular pressure (IOP) in a primate model of glaucoma.

METHODS. A monkey model of experimental glaucoma was combined with immunohistochemical and histochemical methods to assess changes in expression patterns and metabolic activity of cortical neurons in V1.

RESULTS. Experimental unilateral glaucoma altered the spatial and temporal distribution of several neurochemicals associated with cortical plasticity in V1 of the primate. Within-animal comparisons of immunohistochemical studies revealed that GABAa receptor protein and GAP-43 were significantly lower in glaucomatous versus normal eye bands after 2, 4, and 7 months of elevated IOP. SYN immunoreactivity was also lower in the glaucomatous versus the normal eye bands but only at 4 months of elevated IOP. CAMKII immunoreactivity levels were higher in the glaucomatous versus the normal eye bands. Between-animal comparisons revealed that the levels of GAP-43 and SYN were upregulated, whereas levels of GABAa receptor protein were downregulated, in glaucomatous eyes when compared with levels in the visual cortex of normal animals.

CONCLUSIONS. Unilateral elevation of IOP affects both the metabolic activity of cortical neurons and the expressed levels of GAP-43, SYN, GABAa receptor protein, and CAMKII, as measured immunohistochemically in the primary visual cortex of adult monkeys. Because these neurochemicals are thought to be necessary for synaptic plasticity, their redistribution may support functional recovery of cortical neurons after damage to retinal ganglion cells induced by elevated IOP.

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