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Retinal ganglion cell damage in an experimental rodent model of blast-mediated traumatic brain injury
Journal article   Open access   Peer reviewed

Retinal ganglion cell damage in an experimental rodent model of blast-mediated traumatic brain injury

Kabhilan Mohan, Helga Kecova, Elena Hernandez-Merino, Randy H Kardon and Matthew M Harper
Investigative ophthalmology & visual science, Vol.54(5), pp.3440-3450
05/15/2013
DOI: 10.1167/iovs.12-11522
PMCID: PMC4597486
PMID: 23620426
url
https://doi.org/10.1167/iovs.12-11522View
Published (Version of record) Open Access

Abstract

To evaluate retina and optic nerve damage following experimental blast injury. Healthy adult mice were exposed to an overpressure blast wave using a custom-built blast chamber. The effects of blast exposure on retina and optic nerve function and structure were evaluated using the pattern electroretinogram (pERG), spectral domain optical coherence tomography (OCT), and the chromatic pupil light reflex. Assessment of the pupil response to light demonstrated decreased maximum pupil constriction diameter in blast-injured mice using red light or blue light stimuli 24 hours after injury compared with baseline in the eye exposed to direct blast injury. A decrease in the pupil light reflex was not observed chronically following blast exposure. We observed a biphasic pERG decrease with the acute injury recovering by 24 hours postblast and the chronic injury appearing at 4 months postblast injury. Furthermore, at 3 months following injury, a significant decrease in the retinal nerve fiber layer was observed using OCT compared with controls. Histologic analysis of the retina and optic nerve revealed punctate regions of reduced cellularity in the ganglion cell layer and damage to optic nerves. Additionally, a significant upregulation of proteins associated with oxidative stress was observed acutely following blast exposure compared with control mice. Our study demonstrates that decrements in retinal ganglion cell responses can be detected after blast injury using noninvasive functional and structural tests. These objective responses may serve as surrogate tests for higher CNS functions following traumatic brain injury that are difficult to quantify.
Immunohistochemistry Retina - metabolism Male Brain Injuries - metabolism Aldehydes - metabolism Optic Nerve Injuries - diagnosis Retinal Ganglion Cells - metabolism Retinal Ganglion Cells - pathology Blast Injuries - complications Light Amyloid beta-Peptides - metabolism Optic Nerve Injuries - metabolism Disease Models, Animal Electroretinography Optic Nerve Injuries - etiology Tomography, Optical Coherence Mice, Inbred C57BL Brain Injuries - diagnosis Animals Reflex, Pupillary Mice Tears - physiology Brain Injuries - etiology Retina - pathology Retina - injuries Nitric Oxide Synthase Type II - metabolism

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