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YĆ¼cel et al. (209) had previously shown that monocular primate glaucoma had led to decreased parvalbumin-immunoreactive cells in the lateral geniculate nucleus (LGN), the main target for the axons of the retinal ganglion cells. In this study, they examined monkeys with experimental glaucoma, some of which had been treated with the NMDA antagonist memantine. Although they
Memantine protected glaucoma monkey lateral genucleate cells against cell size reductiondid not see significantly decreased cell counts in this study, they did see decreased cell size within the relevant layers of the LGN, particularly in the magnocellular layer. More importantly, the atrophy was less in monkeys treated with memantine, implying that this drug may prevent postsynaptic effects from glaucomatous optic nerves. Whether the drug is acting at the LGN or at the retina in preventing these changes is moot, as it is typically given systemically. The positive effect could be from blocking excitotoxicity, mildly decreasing activity, or inducing BDNF or other proteins. NSAIDs and latanoprost