ArticleFrontiers in neuroscience2019
Impairment of Membrane Repolarization Accompanies Axon Transport Deficits in Glaucoma.
Article in Frontiers in neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- Topical eye treatment with JGRi1, a protein/protein interaction inhibitor, mitigates retinal degeneration.Cell death & disease · 2026Article
- Glaucomatous retinal ganglion cells: death and protection.International journal of ophthalmology · 2025Review
- Article
- Uveitic glaucoma-like features in Yap conditional knockout mice.Cell death discovery · 2024Article
- Retinal ganglion cells adapt to ionic stress in experimental glaucoma.Frontiers in neuroscience · 2023Article
- Axonal Transport Defects in Retinal Ganglion Cell Diseases.Advances in experimental medicine and biology · 2023Review
- Bax Contributes to Retinal Ganglion Cell Dendritic Degeneration During Glaucoma.Molecular neurobiology · 2022Article
- Axon hyperexcitability in the contralateral projection following unilateral optic nerve crush in mice.Brain communications · 2022Article
- Sensitivity to extracellular potassium underlies type-intrinsic differences in retinal ganglion cell excitability.Frontiers in cellular neuroscience · 2022Article
- Interleukin-6 promotes microtubule stability in axons via Stat3 protein-protein interactions.iScience · 2021Article
- Intrinsic Morphologic and Physiologic Development of Human Derived Retinal Ganglion Cells In Vitro.Translational vision science & technology · 2021Article
- Neuroprotection by WldMolecular neurodegeneration · 2021Article
- Therapeutic Drugs and Devices for Tackling Ocular Hypertension and Glaucoma, and Need for Neuroprotection and Cytoprotective Therapies.Frontiers in pharmacology · 2021Review
- Elevated Hydrostatic Pressure Causes Retinal Degeneration Through Upregulating Lipocalin-2.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Glaucoma is a leading cause of blindness worldwide, resulting from degeneration of retinal ganglion cells (RGCs), which form the optic nerve. In glaucoma, axon transport deficits appear to precede structural degeneration of RGC axons. The period of time between the onset of axon transport deficits and the structural degeneration of RGC axons may represent a therapeutic window for the prevention of irreversible vision loss. However, it is unclear how deficits in axon transport relate to the electrophysiological capacity of RGCs to produce and maintain firing frequencies that encode visual stimuli. Here, we examined the electrophysiological signature of individual RGCs in glaucomatous retina with respect to axon transport facility. Utilizing the Microbead Occlusion Model of murine ocular hypertension, we performed electrophysiological recordings of RGCs with and without deficits in anterograde axon transport. We found that RGCs with deficits in axon transport have a reduced ability to maintain spiking frequency that arises from elongation of the repolarization phase of the action potential. This repolarization phenotype arises from reduced cation flux and K+ dyshomeostasis that accompanies pressure-induced decreases in Na/K-ATPase expression and activity.
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Registered trials
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