Nodes of Ranvier in Glaucoma

Neuroscience
Matthew A SmithSamuel D Crish

Abstract

Retinal ganglion cell axons of the DBA/2J mouse model of glaucoma, a model characterized by extensive neuroinflammation, preserve synaptic contacts with their subcortical targets for a time after onset of anterograde axonal transport deficits, axon terminal hypertrophy, and cytoskeletal alterations. Though retrograde axonal transport is still evident in these axons, it is unknown if they retain their ability to transmit visual information to the brain. Using a combination of in vivo multiunit electrophysiology, neuronal tract tracing, multichannel immunofluorescence, and transmission electron microscopy, we report that eye-brain signaling deficits precede transport loss and axonal degeneration in the DBA/2J retinal projection. These deficits are accompanied by node of Ranvier pathology - consisting of increased node length and redistribution of the voltage-gated sodium channel Nav1.6 that parallel changes seen early in multiple sclerosis (MS) axonopathy. Further, with age, axon caliber and neurofilament density increase without corresponding changes in myelin thickness. In contrast to these findings in DBA/2J mice, node pathologies were not observed in the induced microbead occlusion model of glaucoma - a model that lacks pre-e...Continue Reading

Citations

Apr 11, 2020·Frontiers in Physiology·Nolan R McGradyDavid J Calkins
Oct 15, 2019·Frontiers in Cellular Neuroscience·Ashish BhandariMatthew J Van Hook
Mar 23, 2021·Frontiers in Cell and Developmental Biology·Naseem AmirmokhtariMatthew A Smith
Jun 3, 2021·International Journal of Molecular Sciences·Marie ClaesLieve Moons

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