Torsion-Induced Traumatic Optic Neuropathy (TITON): A physiologically relevant animal model of traumatic optic neuropathy.
Traumatic optic neuropathy (TON) is a common cause of irreversible blindness following head injury. TON is characterized by axon damage in the optic nerve followed by retinal ganglion cell death in the days and weeks following injury. At present, no therapeutic or surgical approach has been found to...
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2025-01-01
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| Series: | PLoS ONE |
| Online Access: | https://doi.org/10.1371/journal.pone.0312220 |
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| author | Annie K Ryan Brooke I Asemota Tyler Heisler-Taylor Claire Mello Luis Rodriguez William E Sponsel Julie Racine Tonia S Rex Randolph D Glickman Matthew A Reilly |
| author_facet | Annie K Ryan Brooke I Asemota Tyler Heisler-Taylor Claire Mello Luis Rodriguez William E Sponsel Julie Racine Tonia S Rex Randolph D Glickman Matthew A Reilly |
| author_sort | Annie K Ryan |
| collection | DOAJ |
| description | Traumatic optic neuropathy (TON) is a common cause of irreversible blindness following head injury. TON is characterized by axon damage in the optic nerve followed by retinal ganglion cell death in the days and weeks following injury. At present, no therapeutic or surgical approach has been found to offer any benefit beyond observation alone. This is due in part to the lack of translational animal models suitable for understanding mechanisms and evaluating candidate treatments. In this study, we developed a rat model of TON in which the eye is rapidly rotated, inflicting mechanical stress on the optic nerve and leading to significant visual deficits. These functional deficits were thoroughly characterized up to one week after injury using electrophysiology and immunohistochemistry. The photopic negative response (PhNR) of the light adapted full field electroretinogram (LA ffERG) was significantly altered following injury. This correlated with increased biomarkers of retinal stress, axon disruption, and cell death. Together, this evidence suggests the utility of our model for mimicking clinically relevant TON and that the PhNR may be an early diagnostic for TON. Future studies will utilize this animal model for evaluation of candidate treatments. |
| format | Article |
| id | doaj-art-97599ad5d97447588139a399339f29b0 |
| institution | Kabale University |
| issn | 1932-6203 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj-art-97599ad5d97447588139a399339f29b02025-02-05T05:31:20ZengPublic Library of Science (PLoS)PLoS ONE1932-62032025-01-01201e031222010.1371/journal.pone.0312220Torsion-Induced Traumatic Optic Neuropathy (TITON): A physiologically relevant animal model of traumatic optic neuropathy.Annie K RyanBrooke I AsemotaTyler Heisler-TaylorClaire MelloLuis RodriguezWilliam E SponselJulie RacineTonia S RexRandolph D GlickmanMatthew A ReillyTraumatic optic neuropathy (TON) is a common cause of irreversible blindness following head injury. TON is characterized by axon damage in the optic nerve followed by retinal ganglion cell death in the days and weeks following injury. At present, no therapeutic or surgical approach has been found to offer any benefit beyond observation alone. This is due in part to the lack of translational animal models suitable for understanding mechanisms and evaluating candidate treatments. In this study, we developed a rat model of TON in which the eye is rapidly rotated, inflicting mechanical stress on the optic nerve and leading to significant visual deficits. These functional deficits were thoroughly characterized up to one week after injury using electrophysiology and immunohistochemistry. The photopic negative response (PhNR) of the light adapted full field electroretinogram (LA ffERG) was significantly altered following injury. This correlated with increased biomarkers of retinal stress, axon disruption, and cell death. Together, this evidence suggests the utility of our model for mimicking clinically relevant TON and that the PhNR may be an early diagnostic for TON. Future studies will utilize this animal model for evaluation of candidate treatments.https://doi.org/10.1371/journal.pone.0312220 |
| spellingShingle | Annie K Ryan Brooke I Asemota Tyler Heisler-Taylor Claire Mello Luis Rodriguez William E Sponsel Julie Racine Tonia S Rex Randolph D Glickman Matthew A Reilly Torsion-Induced Traumatic Optic Neuropathy (TITON): A physiologically relevant animal model of traumatic optic neuropathy. PLoS ONE |
| title | Torsion-Induced Traumatic Optic Neuropathy (TITON): A physiologically relevant animal model of traumatic optic neuropathy. |
| title_full | Torsion-Induced Traumatic Optic Neuropathy (TITON): A physiologically relevant animal model of traumatic optic neuropathy. |
| title_fullStr | Torsion-Induced Traumatic Optic Neuropathy (TITON): A physiologically relevant animal model of traumatic optic neuropathy. |
| title_full_unstemmed | Torsion-Induced Traumatic Optic Neuropathy (TITON): A physiologically relevant animal model of traumatic optic neuropathy. |
| title_short | Torsion-Induced Traumatic Optic Neuropathy (TITON): A physiologically relevant animal model of traumatic optic neuropathy. |
| title_sort | torsion induced traumatic optic neuropathy titon a physiologically relevant animal model of traumatic optic neuropathy |
| url | https://doi.org/10.1371/journal.pone.0312220 |
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