June 2013
Volume 54, Issue 15
Free
ARVO Annual Meeting Abstract  |   June 2013
Ocular Blast Trauma in the DBA/2J Mouse
Author Affiliations & Notes
  • Courtney Bricker-Anthony
    Ophthalmology, Vanderbilt University, Nashville, TN
  • Jessica Hines-Beard
    Ophthalmology, Vanderbilt University, Nashville, TN
  • Lauren D'Surney
    Ophthalmology, University of Tennessee Health Science Center, Memphis, TN
  • Eldon Geisert
    Ophthalmology, University of Tennessee Health Science Center, Memphis, TN
  • Tonia Rex
    Ophthalmology, Vanderbilt University, Nashville, TN
  • Footnotes
    Commercial Relationships Courtney Bricker-Anthony, None; Jessica Hines-Beard, None; Lauren D'Surney, None; Eldon Geisert, None; Tonia Rex, PCT/US2012/021247 (P)
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 728. doi:
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    • Get Citation

      Courtney Bricker-Anthony, Jessica Hines-Beard, Lauren D'Surney, Eldon Geisert, Tonia Rex; Ocular Blast Trauma in the DBA/2J Mouse. Invest. Ophthalmol. Vis. Sci. 2013;54(15):728.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: To characterize ocular blast injury in the DBA/2J mouse.

Methods: We exposed the eyes of 3-month-old DBA/2J mice to a single overpressure air wave (blast) produced by a modified paintball marker. Output pressure was measured using a pressure transducer. The mice were placed in a protective housing chamber with only the left eye exposed. Mice experienced a 23, 26, or 30 psi blast. Assessments of intraocular pressure, gross pathology, and visual acuity were performed at 0, 3, 7,14, and 28 days following blast exposure. Optical coherence tomography was performed at 3 days post-blast. Cryo embedded eyes were labeled for anti-GFAP, TUNEL, and anti-Nitrotyrosine. Eyes and optic nerves were embedded in resin and sections were stained with toluidine blue or p-Phenylenediamine, respectively.

Results: Frequency of anterior pole damage increased with time and blast pressure. Commonly observed gross pathologies included corneal edema, corneal neovascularization, and traumatic cataract. Optical coherence tomography imaging revealed retinal detachments at 3 days post-injury. The average percent of retina length with TUNEL positive cells was 24% and 11% after exposure to a 26 psi blast at 3 and 7 days, respectively. Affected cell populations included photoreceptor cells, inner nuclear layer cells, and retinal ganglion cells. GFAP upregulation was observed throughout the retina at both 3 and 7 days. Positive staining for anti-nitrotyrosine was noted in the inner retina of 3 day blast exposed retinas. Additionally, in resin embedded eyes, pyknosis, immune infiltrate, retinal detachments, epiretinal membranes, and subretinal debris were observed. Degenerating axons were present in the optic nerves 28 days post-injury.

Conclusions: The DBA/2J mice are more vulnerable to anterior and posterior pole damage than the C57Bl/6 and Balb/c mice. Differences in responses to blast exposure among inbred mouse strains may be indicative of genetic susceptibility. Immune infiltration was primarily observed in the DBA/2J and is likely due to Anterior Chamber-Associated Immune Deviation, which may contribute to the severity of the phenotype. This mouse model recapitulates commonly observed ocular pathologies in blast-exposed Veterans and may prove useful for testing of potential therapeutics in vivo.

Keywords: 695 retinal degenerations: cell biology • 742 trauma • 494 degenerations/dystrophies  
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