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Brooke Ivie Asemota, Randolph D Glickman, William Eric Sponsel, Matthew Aaron Reilly; Determination of Injury Thresholds for Torsional Indirect Traumatic Optic Neuropathy in a Rat Model. Invest. Ophthalmol. Vis. Sci. 2014;55(13):6194.
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© ARVO (1962-2015); The Authors (2016-present)
Traumatic optic neuropathy (TON) occurs in up to 5% of all head traumas resulting in severe visual deficit or blindness. In this study we imposed torsional indirect TON in a physiologically relevant rat model, which may be used for development of novel therapeutics.
Flash visual evoked potentials (fVEPs) were used before and after injury stimulus to characterize the visual performance of the visual track. A torsional indirect TON insult was applied using a robot described previously (Reilly et al., ARVO 2013 E-abstract 54:5757). The amplitude and velocity of this insult was varied to modulate the degree of irreversible TON. Histopathology was also used to examine optic nerve sections.
Application of super-saccade rotation induced TON (Fig. 1). The torsion parameters correlated with fVEP amplitude and latency (Fig. 2).
The difference between pre- and post-traumatic event fVEPs directly corresponds to optic nerve damage because the signal relay producing the fVEP is dependent on the conductivity of the optic nerve with regards to amplitude, period, and phase number. Because the optic nerve is a part of the Central Nervous System (CNS), the neuroprotectives that are effective in preventing blindness in our TON rat model may be applicable to other neurodegenerative diseases and disorders.
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