Science University Research Symposium (SURS)
Publication Date
2026
College
College of Sciences & Mathematics
Department
Biology, Department of
Presentation Type
Poster Presentation
Abstract
Limited Injury Severity Constrains Therapeutic Evaluation in a Mouse Model of Mild Indirect Traumatic Optic Neuropathy
Christian Corbin, Ching Tzu Yu, Elisabeth Artis, Annie K. Ryan, Sequoia Wade, and Tonia S. Rex
Vanderbilt Eye Institute, Vanderbilt University Medical Center, Nashville, Tennessee, United States
Total (2,372/2500 with spaces)
Purpose: (140)
To evaluate therapeutic effects of Nicotinamide (NMN) and Cyclosporine in a mouse model of mild indirect traumatic optic neuropathy (iTON).
Methods: (915)
Mild iTON induction was accomplished via 3x15 psi air blasts in three-month old C57Bl/6 mice. The animals were anesthetized and placed in a chamber with a hole at the location of the left eye and directly across from the barrel of a customized paintball marker. Mice were treated 2 days post-blast with either NMN (200 mg/kg/day, oral) or Cyclosporine (0.05%, single intravitreal injection). NMN was delivered in their drinking water for 24 hours, and water consumption was tracked. Cyclosporine control mice were injected with buffer. Mice were assessed at baseline and 3 weeks post-blast. To evaluate active axon transport, we injected mice intravitreally with fluorescent cholera toxin B 1 day prior to euthanasia and then quantified fluorescence in the superior colliculus. Bright-field images of optic nerve cross-sections were analyzed to quantify glial area post-blast as an indirect measure of axon damage.
Results: (853)
In this mild model of ITON, we did not detect deficits in axon transport through CTB tracing comparing percent positive stained in SC region at 3weeks (3 blast, 70.52%; sham, 70.98%), despite previously detecting axon damage at 2 weeks post-3 blast exposure. Cyclosporin-treated mice also had similar levels of axon transport compared to sham (72.43%). In contrast, reduced axon transport was detected in the NMN treated mice (60.04%, p=0.035). Next, glial area hypertrophy was detected in the 3 blast non-treated model when compared to sham (Blast, 17.41%; sham, 11.10%). NMN and Cyclosporine treated groups also resulted in a glial area increase when compared to sham (Mean=,21.24%, p= 0.0111;24.10%, p=0.0312, respectively). In a small group of samples, we also detected glial area increase in 6 blast groups when compared to sham (24.10%, p< 0.0001).
Conclusions: (464)
Damage induced by our 3x15 psi blast paradigm was not great enough to inhibit active axon transport but did cause glial hypertrophy in the optic nerve. Glial area was increased in therapeutic groups as well, indicating neither treatment was protective. We detected no therapeutic effects in NMN and Cyclosporine-treated mice in our mild iTON model. Future experiments will revert to the 6-blast paradigm to induce more robust injury to test our treatment groups.
Financial Relationship(s) Disclosure: No financial disclosure
Support: DoW CDMRP HT9425-25-1-0529, NIH NEI R01EY036252, DoW CDMRP HT9425-24-1-0563, Marlene & Spencer Hays Directorship; Ret. MAJ GEN Stephen L. Jones, MD Fund, Potocsnak Family Fund, NIH NEI P30EY008126 (VVRC), RPB Unrestricted Funds (VEI)
Recommended Citation
Corbin, Christian S., "Limited Injury Severity Constrains Therapeutic Evaluation in a Mouse Model of Mild Indirect Traumatic Optic Neuropathy" (2026). Science University Research Symposium (SURS). 390.
https://repository.belmont.edu/surs/390
