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Neurodegeneration and Vision Loss after Mild Blunt Trauma in the C57Bl/6 and DBA/2J Mouse.

Bricker-Anthony C, Rex TS - PLoS ONE (2015)

Bottom Line: Visual acuity decreased over time in both strains, but was more rapid and severe in the DBA/2J.Although our model directs an overpressure air-wave at the left eye in a restrained and otherwise protected mouse, retinal damage was detected in the contralateral eye.Thus we describe a model of mild blunt eye trauma.

View Article: PubMed Central - PubMed

Affiliation: Vanderbilt Eye Institute, Vanderbilt University, Nashville, Tennessee, United States of America; Vanderbilt Brain Institute, Vanderbilt University, Nashville, Tennessee, United States of America.

ABSTRACT
Damage to the eye from blast exposure can occur as a result of the overpressure air-wave (primary injury), flying debris (secondary injury), blunt force trauma (tertiary injury), and/or chemical/thermal burns (quaternary injury). In this study, we investigated damage in the contralateral eye after a blast directed at the ipsilateral eye in the C57Bl/6J and DBA/2J mouse. Assessments of ocular health (gross pathology, electroretinogram recordings, optokinetic tracking, optical coherence tomography and histology) were performed at 3, 7, 14 and 28 days post-trauma. Olfactory epithelium and optic nerves were also examined. Anterior pathologies were more common in the DBA/2J than in the C57Bl/6 and could be prevented with non-medicated viscous eye drops. Visual acuity decreased over time in both strains, but was more rapid and severe in the DBA/2J. Retinal cell death was present in approximately 10% of the retina at 7 and 28 days post-blast in both strains. Approximately 60% of the cell death occurred in photoreceptors. Increased oxidative stress and microglial reactivity was detected in both strains, beginning at 3 days post-injury. However, there was no sign of injury to the olfactory epithelium or optic nerve in either strain. Although our model directs an overpressure air-wave at the left eye in a restrained and otherwise protected mouse, retinal damage was detected in the contralateral eye. The lack of damage to the olfactory epithelium and optic nerve, as well as the different timing of cell death as compared to the blast-exposed eye, suggests that the injuries were due to physical contact between the contralateral eye and the housing chamber of the blast device and not propagation of the blast wave through the head. Thus we describe a model of mild blunt eye trauma.

No MeSH data available.


Related in: MedlinePlus

Blast causes ERG deficits in the D2, but not the Bl/6.(A,C,E) Graphs of the average ± SEM of amax (A), bmax (C) and oscillatory potentials (E) for the Bl/6 mice at baseline, 7dpi and 28 dpi. (B, D, F) Graphs of the average ± SEM of amax (B), bmax (D) and oscillatory potentials (F) for the D2 mice at baseline, 7dpi and 28 dpi. *p<0.05.
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pone.0131921.g012: Blast causes ERG deficits in the D2, but not the Bl/6.(A,C,E) Graphs of the average ± SEM of amax (A), bmax (C) and oscillatory potentials (E) for the Bl/6 mice at baseline, 7dpi and 28 dpi. (B, D, F) Graphs of the average ± SEM of amax (B), bmax (D) and oscillatory potentials (F) for the D2 mice at baseline, 7dpi and 28 dpi. *p<0.05.

Mentions: There were no significant changes in the ERG amax, bmax or oscillatory potentials at any time point assessed in the Bl/6 eye (n = 22) after injury (Fig 12A, 12C and 12E). However, there were significant reductions in both amax and bmax in the D2 (n = 26) after blast when compared to baseline values (Fig 12B and 12D). At 7 dpi, the amax was significantly lower than baseline at light intensities that correlate with daytime light levels. At 0 log cd*s/m2 the amax was decreased by 39% from 135.7 ± 9.6 μV at baseline to 82.5 ± 14.2 μV, p<0.01 (Fig 12B). At 1 log cd*s/m2 the amax was decreased by 29% from 194.3 ± 12.2 μV to 137.9 ± 20.2 μV, p<0.05 (Fig 12B). At 28 dpi, the amax recovered, but the bmax was significantly reduced at several light intensities. At -1 log cd*s/m2 the bmax was decreased 44% from 299.0 ± 17.1 μV to 168.9 ± 35.8 μV, p<0.01 (Fig 12E). At 1 log cd*s/m2 the bmax was decreased 46% from 257.0 ± 17.1 μV at baseline to 137.7 ± 21.1 μV, p<0.01 (Fig 12E). The oscillatory potentials did not change after blast in the D2 (Fig 12E).


Neurodegeneration and Vision Loss after Mild Blunt Trauma in the C57Bl/6 and DBA/2J Mouse.

Bricker-Anthony C, Rex TS - PLoS ONE (2015)

Blast causes ERG deficits in the D2, but not the Bl/6.(A,C,E) Graphs of the average ± SEM of amax (A), bmax (C) and oscillatory potentials (E) for the Bl/6 mice at baseline, 7dpi and 28 dpi. (B, D, F) Graphs of the average ± SEM of amax (B), bmax (D) and oscillatory potentials (F) for the D2 mice at baseline, 7dpi and 28 dpi. *p<0.05.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4493046&req=5

pone.0131921.g012: Blast causes ERG deficits in the D2, but not the Bl/6.(A,C,E) Graphs of the average ± SEM of amax (A), bmax (C) and oscillatory potentials (E) for the Bl/6 mice at baseline, 7dpi and 28 dpi. (B, D, F) Graphs of the average ± SEM of amax (B), bmax (D) and oscillatory potentials (F) for the D2 mice at baseline, 7dpi and 28 dpi. *p<0.05.
Mentions: There were no significant changes in the ERG amax, bmax or oscillatory potentials at any time point assessed in the Bl/6 eye (n = 22) after injury (Fig 12A, 12C and 12E). However, there were significant reductions in both amax and bmax in the D2 (n = 26) after blast when compared to baseline values (Fig 12B and 12D). At 7 dpi, the amax was significantly lower than baseline at light intensities that correlate with daytime light levels. At 0 log cd*s/m2 the amax was decreased by 39% from 135.7 ± 9.6 μV at baseline to 82.5 ± 14.2 μV, p<0.01 (Fig 12B). At 1 log cd*s/m2 the amax was decreased by 29% from 194.3 ± 12.2 μV to 137.9 ± 20.2 μV, p<0.05 (Fig 12B). At 28 dpi, the amax recovered, but the bmax was significantly reduced at several light intensities. At -1 log cd*s/m2 the bmax was decreased 44% from 299.0 ± 17.1 μV to 168.9 ± 35.8 μV, p<0.01 (Fig 12E). At 1 log cd*s/m2 the bmax was decreased 46% from 257.0 ± 17.1 μV at baseline to 137.7 ± 21.1 μV, p<0.01 (Fig 12E). The oscillatory potentials did not change after blast in the D2 (Fig 12E).

Bottom Line: Visual acuity decreased over time in both strains, but was more rapid and severe in the DBA/2J.Although our model directs an overpressure air-wave at the left eye in a restrained and otherwise protected mouse, retinal damage was detected in the contralateral eye.Thus we describe a model of mild blunt eye trauma.

View Article: PubMed Central - PubMed

Affiliation: Vanderbilt Eye Institute, Vanderbilt University, Nashville, Tennessee, United States of America; Vanderbilt Brain Institute, Vanderbilt University, Nashville, Tennessee, United States of America.

ABSTRACT
Damage to the eye from blast exposure can occur as a result of the overpressure air-wave (primary injury), flying debris (secondary injury), blunt force trauma (tertiary injury), and/or chemical/thermal burns (quaternary injury). In this study, we investigated damage in the contralateral eye after a blast directed at the ipsilateral eye in the C57Bl/6J and DBA/2J mouse. Assessments of ocular health (gross pathology, electroretinogram recordings, optokinetic tracking, optical coherence tomography and histology) were performed at 3, 7, 14 and 28 days post-trauma. Olfactory epithelium and optic nerves were also examined. Anterior pathologies were more common in the DBA/2J than in the C57Bl/6 and could be prevented with non-medicated viscous eye drops. Visual acuity decreased over time in both strains, but was more rapid and severe in the DBA/2J. Retinal cell death was present in approximately 10% of the retina at 7 and 28 days post-blast in both strains. Approximately 60% of the cell death occurred in photoreceptors. Increased oxidative stress and microglial reactivity was detected in both strains, beginning at 3 days post-injury. However, there was no sign of injury to the olfactory epithelium or optic nerve in either strain. Although our model directs an overpressure air-wave at the left eye in a restrained and otherwise protected mouse, retinal damage was detected in the contralateral eye. The lack of damage to the olfactory epithelium and optic nerve, as well as the different timing of cell death as compared to the blast-exposed eye, suggests that the injuries were due to physical contact between the contralateral eye and the housing chamber of the blast device and not propagation of the blast wave through the head. Thus we describe a model of mild blunt eye trauma.

No MeSH data available.


Related in: MedlinePlus