• Najiba Mammadova, Shivani Ghaisas, Gary Zenitsky, Donald S Sakaguchi, Anumantha G Kanthasamy, Justin J Greenlee, and M Heather West Greenlee.
• Department of Genetics, Development and Cell Biology, Iowa State University, Ames, Iowa; Immunobiology Graduate Program, Iowa State University, Ames, Iowa; Neuroscience Graduate Program, Iowa State University, Ames, Iowa.
• Am. J. Pathol. 2017 Jul 1; 187 (7): 1459-1472.

AbstractTraumatic brain injury due to blast exposure is currently the most prevalent of war injuries. Although secondary ocular blast injuries due to flying debris are more common, primary ocular blast exposure resulting from blast wave pressure has been reported among survivors of explosions, but with limited understanding of the resulting retinal pathologies. Using a compressed air-driven shock tube system, adult male and female C57BL/6 mice were exposed to blast wave pressure of 300 kPa (43.5 psi) per day for 3 successive days, and euthanized 30 days after injury. We assessed retinal tissues using immunofluorescence for glial fibrillary acidic protein, microglia-specific proteins Iba1 and CD68, and phosphorylated tau (AT-270 pThr181 and AT-180 pThr231). Primary blast wave pressure resulted in activation of Müller glia, loss of photoreceptor cells, and an increase in phosphorylated tau in retinal neurons and glia. We found that 300-kPa blasts yielded no detectable cognitive or motor deficits, and no neurochemical or biochemical evidence of injury in the striatum or prefrontal cortex, respectively. These changes were detected 30 days after blast exposure, suggesting the possibility of long-lasting retinal injury and neuronal inflammation after primary blast exposure.Copyright © 2017 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.

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