ArticleProceedings of the National Academy of Sciences of the United States of America2018
Axogenic mechanism enhances retinal ganglion cell excitability during early progression in glaucoma.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.
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Who cites it
89 citing papers in PubMed, 120 citations in OpenAlex.
- Article
- The 5-HT1A receptor antagonist WAY-100635 maleate promotes retinal ganglion cell differentiation and protects the retino-visual circuits.Communications medicine · 2026Article
- Synaptic control of retinal ganglion cell survival and axon regeneration.Molecular neurodegeneration · 2026Review
- Evaluating Increment and Decrement Stimuli Responses in Patients with Glaucoma Using Virtual Reality-Based Perimetry.Ophthalmology science · 2026Article
- Prospects for Neuroprotective Therapies in Glaucoma: Drug Targets and Emerging Clinical Strategies.Drug design, development and therapy · 2026Review
- AKAP1 regulates mitochondrial and synaptic homeostasis to enable neuroprotection and repair in retinal ganglion cell degeneration.bioRxiv : the preprint server for biology · 2025Article
- Restoring AIBP expression in the retina provides neuroprotection in glaucoma.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- The Effect of Advancing Age and Intraocular Pressure Injury on Retinal Ganglion Cell Function and Synaptic Connectivity.Aging cell · 2025Article
- Enhanced Synaptic Inhibition in the Dorsolateral Geniculate Nucleus in a Mouse Model of Glaucoma.eNeuro · 2024Article
- A novel function and mechanism of ischemia-induced retinal astrocyte-derived exosomes for RGC apoptosis of ischemic retinopathy.Molecular therapy. Nucleic acids · 2024Article
- Long-term HIF-1α stabilization reduces respiration, promotes mitophagy, and results in retinal cell death.Scientific reports · 2023Article
- Neutral sphingomyelinase inhibition promotes local and network degeneration in vitro and in vivo.Cell communication and signaling : CCS · 2023Article
- Large-scale survey of excitatory synapses reveals sublamina-specific and asymmetric synapse disassembly in a neurodegenerative circuit.iScience · 2023Article
- L- and T-type CaNeural regeneration research · 2023Article
- Comparison of Ganglion Cell Layer and Inner Plexiform Layer Rates of Change in Suspected and Established Glaucoma.American journal of ophthalmology · 2023Article
- Microfluidic Platforms Promote Polarization of Human-Derived Retinal Ganglion Cells That Model Axonopathy.Translational vision science & technology · 2023Article
- Retinal ganglion cells adapt to ionic stress in experimental glaucoma.Frontiers in neuroscience · 2023Article
- Retinal TRP channels: Cell-type-specific regulators of retinal homeostasis and multimodal integration.Progress in retinal and eye research · 2023Review
- Preferential Loss of Contrast Decrement Responses in Human Glaucoma.Investigative ophthalmology & visual science · 2022Article
- Time-Frequency Analysis of ERG With Discrete Wavelet Transform and Matching Pursuits for Glaucoma.Translational vision science & technology · 2022Article
29 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Diseases of the brain involve early axon dysfunction that often precedes outright degeneration. Pruning of dendrites and their synapses represents a potential driver of axonopathy by reducing activity. Optic nerve degeneration in glaucoma, the world's leading cause of irreversible blindness, involves early stress to retinal ganglion cell (RGC) axons from sensitivity to intraocular pressure (IOP). This sensitivity also influences survival of RGC dendrites and excitatory synapses in the retina. Here we tested in individual RGCs identified by type the relationship between dendritic organization and axon signaling to light following modest, short-term elevations in pressure. We found dendritic pruning occurred early, by 2 wk of elevation, and independent of whether the RGC responded to light onset (ON cells) or offset (OFF cells). Pruning was similarly independent of ON and OFF in the DBA/2J mouse, a chronic glaucoma model. Paradoxically, all RGCs, even those with significant pruning, demonstrated a transient increase in axon firing in response to the preferred light stimulus that occurred on a backdrop of generally enhanced excitability. The increased response was not through conventional presynaptic signaling, but rather depended on voltage-sensitive sodium channels that increased transiently in the axon. Pruning, axon dysfunction, and deficits in visual acuity did not progress between 2 and 4 wk of elevation. These results suggest neurodegeneration in glaucoma involves an early axogenic response that counters IOP-related stress to excitatory dendritic architecture to slow progression and maintain signaling to the brain. Thus, short-term exposure to elevated IOP may precondition the neural system to further insult.
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