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Tonia Rex, Andrea Elberger, Yunping Deng, Natalie Guley, Jessica Hines-Beard, Lauren D'Surney, Nobel Del Mar, Marcia Honig, Anton Reiner; Visual Deficits in Mice after Mild Traumatic Brain Injury Produced using A Novel Closed-head Model of Primary Overpressure Blast. Invest. Ophthalmol. Vis. Sci. 2013;54(15):5095.
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We have developed a blast model of closed-head mild traumatic brain injury (TBI) in mice using an air pressure wave delivered to one side of the head. Since individuals who have experienced mild TBI frequently suffer from visual impairments, we examined the effects of the blasts on the visual system in our model.
Anesthetized 3-month old C57BL/6 male mice were secured within a mouse holder, and air pressure blasts were delivered to a 7.5 mm diameter area on the left side of the skull between eye and ear. Optomotor testing was used to assess visual acuity and contrast sensitivity, and anatomical methods were used to assess injury to the optic nerve and tract (NeuroSilver, and thin plastic sections), and to visual cortex (immunolabeling for neuronal and glial markers) one month after blast.
No brain pathology or visual impairments were seen in mice after 0-20 psi blasts. By contrast, after 50-60 psi blasts, diffuse axonal injury and brain swelling were observed, but there was no overt cerebral damage. Neurons expressing the immediate early gene cfos were, however, greatly increased in abundance in visual cortex on both sides, indicative of aberrant cortical function after TBI. Axonal degeneration was common in the left optic nerve and its continuation as the right optic tract, and occasionally in the right optic nerve and left optic tract. The right eye showed decreased visual acuity, whereas acuity for the left eye was normal. Both eyes, however, exhibited poorer contrast sensitivity. Since blasts were to the left hemisphere, which receives visual information mainly from the right eye, our results indicate that the 50-60 psi blasts produced sufficiently greater disruption in visual areas of the left side of the brain to preferentially affect right eye acuity performance. Optic nerve damage alone was insufficient to produce an acuity defect for the eye of origin. Contrast sensitivity, however, appears to be more sensitive to optic nerve injury, and the bilateral defects in contrast sensitivity are likely thus to stem from bilateral injury to optic nerves, or central visual areas, or both.
Our mouse model recapitulates the central visual system injury and visual abnormalities that occur after mild forebrain TBI, and thus provides a tool by which to explore its mechanistic basis, and develop therapeutic approaches.
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