ArticleTranslational vision science & technology2021
RGC and Vision Loss From Traumatic Optic Neuropathy Induced by Repetitive Closed Head Trauma Is Dependent on Timing and Force of Impact.
Article in Translational vision science & technology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- Extrinsic Regulation of Optic Nerve Axon Regeneration in the Adult Central Nervous System.Cells · 2026Review
- Reduction of Lipid Droplets Modulates the Injury Response and Enhances CNTF-Induced Axon Regeneration Following Optic Nerve Crush.Molecular neurobiology · 2026Article
- The Role of Nrf2 in SIRT1-Mediated RGC Neuroprotection in Traumatic Optic Neuropathy.Translational vision science & technology · 2026Article
- Stem cells ameliorate neurotrauma-induced visual disturbances and retinal degeneration via broad normalization of β-catenin-related signaling.International journal of medical sciences · 2026Article
- Torsion-Induced Traumatic Optic Neuropathy (TITON): A Physiologically Relevant Animal Model of Traumatic Optic Neuropathy.bioRxiv : the preprint server for biology · 2025Article
- Injective hydrogel encapsulating dental pulp stem cells for the treatment of traumatic optic nerve injury.Frontiers in bioengineering and biotechnology · 2025Article
- Torsion-Induced Traumatic Optic Neuropathy (TITON): A physiologically relevant animal model of traumatic optic neuropathy.PloS one · 2025Article
- Pharmacological Activation and Transgenic Overexpression of SIRT1 Attenuate Traumatic Optic Neuropathy Induced by Blunt Head Impact.Translational vision science & technology · 2024Article
- Comparative Proteomic Study of Retinal Ganglion Cells Undergoing Various Types of Cellular Stressors.bioRxiv : the preprint server for biology · 2024Article
- Comparison of SNCG and NEFH Promoter-Driven Expression of Human SIRT1 Expression in a Mouse Model of Glaucoma.Translational vision science & technology · 2024Article
- Oxidative Stress: A Suitable Therapeutic Target for Optic Nerve Diseases?Antioxidants (Basel, Switzerland) · 2023Review
- Diffusion basis spectrum imaging detects subclinical traumatic optic neuropathy in a closed-head impact mouse model of traumatic brain injury.Frontiers in neurology · 2023Article
- Oxidative stress in the brain and retina after traumatic injury.Frontiers in neuroscience · 2023Review
- Repeat Brn3a immunolabeling rescues faded staining and improves detection of retinal ganglion cells.Experimental eye research · 2023Article
- Inhibition of ferroptosis promotes retina ganglion cell survival in experimental optic neuropathies.Redox biology · 2022Article
- The outcome of surgical and non-surgical treatments for traumatic optic neuropathy: a comparative study of 685 cases.Annals of translational medicine · 2022Article
- Subtype-specific survival and regeneration of retinal ganglion cells in response to injury.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Purpose: Traumatic optic neuropathy (TON) is often caused by blunt head trauma and has no currently effective treatment. Common animal models of TON induced by surgical crush injury are plagued by variability and do not mimic typical mechanisms of TON injury. Traumatic head impact models have recently shown evidence of TON, but the degree of head impact necessary to consistently induce TON is not well characterized, and it is examined here. Methods: Traumatic skull impacts to C57BL/6J mice were induced using an electromagnetic controlled impact device. One impact performed at two depths (mild and severe), as well as three and five repetitive impacts with an interconcussion interval of 48 hours, were tested. Optokinetic responses (OKRs) and retinal ganglion cell (RGC) loss were measured. Results: Five repetitive mild impacts significantly decreased OKR scores and RGC numbers compared with control mice 10 weeks after initial impact, with maximal pathology observed by 6 weeks and partial but significant loss present by 3 weeks. One severe impact induced similar TON. Three mild impacts also induced early OKR and RGC loss, but one mild impact did not. Equivalent degrees of TON were induced bilaterally, and a significant correlation was observed between OKR scores and RGC numbers. Conclusions: Repetitive, mild closed head trauma in mice induces progressive RGC and vision loss that worsens with increasing impacts. Translational Relevance: Results detail a reproducible model of TON that provides a reliable platform for studying potential treatments over a 3- to 6-week time course.
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