title: Retinal ganglion cell damage in an experimental rodent model of blast-mediated traumatic brain injury.
abstract: OBJECTIVE
  To evaluate retina and optic nerve damage following experimental blast injury.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Iowa City Veterans Administration Center for the Prevention and Treatment of Visual Loss, Iowa City, IA, USA. kabhilan@gmail.com
authors.forename: Kabhilan
authors.initials: K
authors.lastname: Mohan
authors.forename: Helga
authors.initials: H
authors.lastname: Kecova
authors.forename: Elena
authors.initials: E
authors.lastname: Hernandez-Merino
authors.forename: Randy H
authors.initials: RH
authors.lastname: Kardon
authors.forename: Matthew M
authors.initials: MM
authors.lastname: Harper
mesh_terms: D000447:Aldehydes / Q000378:metabolism; D016229:Amyloid beta-Peptides / Q000378:metabolism; D000818:Animals; D001753:Blast Injuries / Q000150:complications*; D001930:Brain Injuries / Q000175:diagnosis / Q000209:etiology* / Q000378:metabolism; D004195:Disease Models, Animal; D004596:Electroretinography; D007150:Immunohistochemistry; D008027:Light; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D020221:Optic Nerve Injuries / Q000175:diagnosis / Q000209:etiology* / Q000378:metabolism; D012025:Reflex, Pupillary; D012160:Retina / Q000293:injuries* / Q000378:metabolism / Q000473:pathology; D012165:Retinal Ganglion Cells / Q000378:metabolism / Q000473:pathology*; D013666:Tears / Q000502:physiology; D041623:Tomography, Optical Coherence
chemical_list: D000447:Aldehydes; D016229:Amyloid beta-Peptides; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse; C027576:4-hydroxy-2-nonenal
keywords: blast injury; pattern electroretinography; traumatic brain injury; traumatic optic neuropathy