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Hains and Waxman (1053) studied not just protection of retinal ganglion cells, i.e., neuroprotection, but also their axons, i.e., axoprotection with the sodium channel blocker phenytoin in a rat experimental glaucoma (episcleral vein cautery) model. This extends the work of Naskar and colleagues in the optic nerve crush model and the Waxman group in the experimental allergic encephalomyelitis model, all with phenytoin. They found robust protection of RGC cell bodies (measured by retrograde labeling) with phenytoin, but interestingly, less axonal loss than RGC cell body loss in untreated animals, making it difficult to determine whether the drug truly protected just the axons, or primarily the cell bodies. Nonetheless, this adds to a very small number of studies concerning axoprotection, the next major front line in the war against glaucomatous optic neuropathy.