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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

GFAP labeling is increased in the Müller glia of D2 eyes at 3 and 7 dpi.Low and high magnification epifluourescence micrographs of (A) control, (B) 3 dpi, (C) 7 dpi, and (D) 28 dpi retinas labeled with GFAP (green) and DAPI (blue). The scale bar for the high magnification micrographs is 50μm. The scale bar for the low magnification micrographs is 250μm.
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pone.0131921.g008: GFAP labeling is increased in the Müller glia of D2 eyes at 3 and 7 dpi.Low and high magnification epifluourescence micrographs of (A) control, (B) 3 dpi, (C) 7 dpi, and (D) 28 dpi retinas labeled with GFAP (green) and DAPI (blue). The scale bar for the high magnification micrographs is 50μm. The scale bar for the low magnification micrographs is 250μm.

Mentions: As in the blast-exposed Bl/6 retina, Müller glia remained non-reactive at all time points (control n = 5, 3 dpi n = 6, 7 dpi n = 3 and 28 dpi n = 5), e.g. GFAP immunolabeling was restricted to the astrocytes and Müller glia endfeet (S2 Fig). In contrast, GFAP immunolabeling extended up the Müller cell processes in the D2 retinas (Fig 8B and 8C). At 3 dpi (n = 3), the GFAP positive processes were detected uniformly across the retina (Fig 8B). Treatment with non-medicated eye drops immediately post-blast reduced GFAP labeling to small patches in the mid-peripheral and central retina at 3 dpi (n = 4) (S3B Fig). At 7 dpi (n = 3), GFAP positive processes were only detected in small patches in the mid-peripheral and central retina (Fig 8C). Increased GFAP immunolabeling was not detected in any region of the retina at 28 dpi (n = 6) (Fig 8D).


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

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

GFAP labeling is increased in the Müller glia of D2 eyes at 3 and 7 dpi.Low and high magnification epifluourescence micrographs of (A) control, (B) 3 dpi, (C) 7 dpi, and (D) 28 dpi retinas labeled with GFAP (green) and DAPI (blue). The scale bar for the high magnification micrographs is 50μm. The scale bar for the low magnification micrographs is 250μm.
© Copyright Policy
Related In: Results  -  Collection

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

pone.0131921.g008: GFAP labeling is increased in the Müller glia of D2 eyes at 3 and 7 dpi.Low and high magnification epifluourescence micrographs of (A) control, (B) 3 dpi, (C) 7 dpi, and (D) 28 dpi retinas labeled with GFAP (green) and DAPI (blue). The scale bar for the high magnification micrographs is 50μm. The scale bar for the low magnification micrographs is 250μm.
Mentions: As in the blast-exposed Bl/6 retina, Müller glia remained non-reactive at all time points (control n = 5, 3 dpi n = 6, 7 dpi n = 3 and 28 dpi n = 5), e.g. GFAP immunolabeling was restricted to the astrocytes and Müller glia endfeet (S2 Fig). In contrast, GFAP immunolabeling extended up the Müller cell processes in the D2 retinas (Fig 8B and 8C). At 3 dpi (n = 3), the GFAP positive processes were detected uniformly across the retina (Fig 8B). Treatment with non-medicated eye drops immediately post-blast reduced GFAP labeling to small patches in the mid-peripheral and central retina at 3 dpi (n = 4) (S3B Fig). At 7 dpi (n = 3), GFAP positive processes were only detected in small patches in the mid-peripheral and central retina (Fig 8C). Increased GFAP immunolabeling was not detected in any region of the retina at 28 dpi (n = 6) (Fig 8D).

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