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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

RIP1 and RIP3 immunolabeling increases after injury in both the Bl/6 and D2.Confocal micrographs of retinas from Bl/6 and D2 control eyes (A,B), Bl/6 and D2 3 dpi eyes (C,D) and Bl/6 and D2 28 dpi eyes (E,F). The scale bar in (A) is 50μm and applies to all micrographs.
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pone.0131921.g006: RIP1 and RIP3 immunolabeling increases after injury in both the Bl/6 and D2.Confocal micrographs of retinas from Bl/6 and D2 control eyes (A,B), Bl/6 and D2 3 dpi eyes (C,D) and Bl/6 and D2 28 dpi eyes (E,F). The scale bar in (A) is 50μm and applies to all micrographs.

Mentions: In both Bl/6 and D2 control retinas, RIP1 localized primarily to the Müller glia, the INL, and the inner plexiform layer (IPL), with some light staining in the outer plexiform layer (OPL) (Fig 6A and 6B). RIP3 immunolabeling was present in the IPL and INL in control retinas from both strains (Fig 6A and 6B). At all time points post-injury, changes in RIP1 and RIP3 immunolabeling remained focal (e.g. limited to 3–4 sections per eye).


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

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

RIP1 and RIP3 immunolabeling increases after injury in both the Bl/6 and D2.Confocal micrographs of retinas from Bl/6 and D2 control eyes (A,B), Bl/6 and D2 3 dpi eyes (C,D) and Bl/6 and D2 28 dpi eyes (E,F). The scale bar in (A) is 50μm and applies to all micrographs.
© Copyright Policy
Related In: Results  -  Collection

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

pone.0131921.g006: RIP1 and RIP3 immunolabeling increases after injury in both the Bl/6 and D2.Confocal micrographs of retinas from Bl/6 and D2 control eyes (A,B), Bl/6 and D2 3 dpi eyes (C,D) and Bl/6 and D2 28 dpi eyes (E,F). The scale bar in (A) is 50μm and applies to all micrographs.
Mentions: In both Bl/6 and D2 control retinas, RIP1 localized primarily to the Müller glia, the INL, and the inner plexiform layer (IPL), with some light staining in the outer plexiform layer (OPL) (Fig 6A and 6B). RIP3 immunolabeling was present in the IPL and INL in control retinas from both strains (Fig 6A and 6B). At all time points post-injury, changes in RIP1 and RIP3 immunolabeling remained focal (e.g. limited to 3–4 sections per eye).

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