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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

Caspase-1 immunolabeling increases at 28 dpi in the Bl/6 retina.Epifluorescence micrographs of retinas from control (A), 3 dpi (B) and 28 dpi (C) eyes labeled with anti-caspase-1 (green) and DAPI (blue). Caspase-1 immunolabeling at 28dpi is the same in both central (D) and mid-peripheral (E) retina. The scale bar is 50μm in (A-C) and 250μm in (D) and (E).
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pone.0131921.g007: Caspase-1 immunolabeling increases at 28 dpi in the Bl/6 retina.Epifluorescence micrographs of retinas from control (A), 3 dpi (B) and 28 dpi (C) eyes labeled with anti-caspase-1 (green) and DAPI (blue). Caspase-1 immunolabeling at 28dpi is the same in both central (D) and mid-peripheral (E) retina. The scale bar is 50μm in (A-C) and 250μm in (D) and (E).

Mentions: Caspase-1 immunolabeling was absent in control (n = 3) and 3 dpi Bl/6 retinas (n = 3) (Fig 7A and 7B). In contrast, the majority of 28 dpi Bl/6 retinas (n = 4) exhibited caspase-1 labeling in sparse cells at the inner edge of the INL and in the GCL (Fig 7C). The caspase-1 positive cells were present throughout the retina (Fig 7D and 7E). In the D2, caspase-1 positive cells were present within the INL and GCL of controls (n = 3) (S1A Fig). However, the caspase-1 labeling decreased after trauma such that no labeling was present at either 3 (n = 3) or 28 dpi (n = 3) (S1B–S1C Fig).


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

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

Caspase-1 immunolabeling increases at 28 dpi in the Bl/6 retina.Epifluorescence micrographs of retinas from control (A), 3 dpi (B) and 28 dpi (C) eyes labeled with anti-caspase-1 (green) and DAPI (blue). Caspase-1 immunolabeling at 28dpi is the same in both central (D) and mid-peripheral (E) retina. The scale bar is 50μm in (A-C) and 250μm in (D) and (E).
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4493046&req=5

pone.0131921.g007: Caspase-1 immunolabeling increases at 28 dpi in the Bl/6 retina.Epifluorescence micrographs of retinas from control (A), 3 dpi (B) and 28 dpi (C) eyes labeled with anti-caspase-1 (green) and DAPI (blue). Caspase-1 immunolabeling at 28dpi is the same in both central (D) and mid-peripheral (E) retina. The scale bar is 50μm in (A-C) and 250μm in (D) and (E).
Mentions: Caspase-1 immunolabeling was absent in control (n = 3) and 3 dpi Bl/6 retinas (n = 3) (Fig 7A and 7B). In contrast, the majority of 28 dpi Bl/6 retinas (n = 4) exhibited caspase-1 labeling in sparse cells at the inner edge of the INL and in the GCL (Fig 7C). The caspase-1 positive cells were present throughout the retina (Fig 7D and 7E). In the D2, caspase-1 positive cells were present within the INL and GCL of controls (n = 3) (S1A Fig). However, the caspase-1 labeling decreased after trauma such that no labeling was present at either 3 (n = 3) or 28 dpi (n = 3) (S1B–S1C Fig).

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