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Morris L. J. Crawford, Ronald S. Harwerth, Earl L. Smith, Fran Shen, Louvenia Carter–Dawson; Glaucoma in Primates: Cytochrome Oxidase Reactivity in Parvo- and Magnocellular Pathways. Invest. Ophthalmol. Vis. Sci. 2000;41(7):1791-1802.
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purpose. To evaluate the differential effects of ganglion cell depletion from
experimental glaucoma on the relative metabolic activities of neurons
in the parvo (P)- and magno (M)-cellular visual pathways of the macaque
methods. Monocular experimental glaucoma was induced in monkeys (Macaca
mulatta and M. fascicularis) by applying a laser to the
trabecular meshwork to increase intraocular pressure (IOP). After other
behavioral and electrophysiological studies, the lateral geniculate
nuclei (LGNs) and the primary visual cortices were analyzed for
functional afference from surviving ganglion cells, indicated by
cytochrome oxidase (CO) histochemistry.
results. CO reactivity (COR) indicated a general reduction in neural metabolism
with increasing severity of glaucoma. COR in the LGNs was reduced to
the same degree in both the P- and M-cellular layers. In layer 4Cβ of
the V1 cortex, the reactivity was always reduced more than in the layer
conclusions. Experimental glaucoma in monkeys reduces visual afference to the
central nervous system, thereby reducing the metabolic drive as
indicated by COR. The detrimental effect of glaucoma did not appear to
be any greater for the M-cell, rather than the P-cell pathway in the
LGN or in the visual cortex. Both are affected by the duration and
severity of the experimental glaucoma. Overall, the alterations in
metabolism of neurons in the parallel visual pathways supplied by the
Pα and Pβ ganglion cells do not suggest that tests based on the
functional properties of one or the other would provide optimal
assessment of glaucoma.
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