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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

The ocular surface of the D2 eye is injured.(A) Calcium deposits (arrow) are common in the normal D2 eye. (B) Hyphema (arrow), corneal edema and a cataract at 3 dpi. (C) Corneal edema and calcium deposits (arrow) at 7 dpi. (D) Corneal edema, corneal neovascularization and calcium deposits at 14 dpi. (E) A corneal scar and corneal neovascularization (arrow) at 28 dpi.
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pone.0131921.g001: The ocular surface of the D2 eye is injured.(A) Calcium deposits (arrow) are common in the normal D2 eye. (B) Hyphema (arrow), corneal edema and a cataract at 3 dpi. (C) Corneal edema and calcium deposits (arrow) at 7 dpi. (D) Corneal edema, corneal neovascularization and calcium deposits at 14 dpi. (E) A corneal scar and corneal neovascularization (arrow) at 28 dpi.

Mentions: No anterior pathology was detected in the Bl/6 eye, consistent with results in the blast-exposed eye and naïve controls.[8] In the D2 eye, corneal edema occurred in 52% of eyes at 3 days dpi (n = 27) and remained in 43% of mice at 28 dpi (n = 7, Fig 1B). Cataracts were observed in 30% of D2 eyes at both 3 and 28 dpi (Fig 1B). Pathologies that became more prevalent later included corneal neovascularization and corneal calcifications. Corneal neovascularization was detected in 44% and 29% of eyes at 14 (n = 9) and 28 dpi, respectively (Fig 1D and 1E). Corneal calcification was detected in 33% and 43% of eyes at 14 and 28 dpi, respectively (Fig 1E). Note that calcium deposits in the cornea were present in many of the D2 blast and naïve control mice as a normal finding for this strain (Fig 1C and 1D) [15]. Similar to our previous results in the blast-exposed eye, treatment with non-medicated eye drops prevented all of the corneal pathology. Thus, we treated all following mice with non-medicated eye drops to prevent corneal pathology, unless otherwise stated in order to test visual function.


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

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

The ocular surface of the D2 eye is injured.(A) Calcium deposits (arrow) are common in the normal D2 eye. (B) Hyphema (arrow), corneal edema and a cataract at 3 dpi. (C) Corneal edema and calcium deposits (arrow) at 7 dpi. (D) Corneal edema, corneal neovascularization and calcium deposits at 14 dpi. (E) A corneal scar and corneal neovascularization (arrow) at 28 dpi.
© Copyright Policy
Related In: Results  -  Collection

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

pone.0131921.g001: The ocular surface of the D2 eye is injured.(A) Calcium deposits (arrow) are common in the normal D2 eye. (B) Hyphema (arrow), corneal edema and a cataract at 3 dpi. (C) Corneal edema and calcium deposits (arrow) at 7 dpi. (D) Corneal edema, corneal neovascularization and calcium deposits at 14 dpi. (E) A corneal scar and corneal neovascularization (arrow) at 28 dpi.
Mentions: No anterior pathology was detected in the Bl/6 eye, consistent with results in the blast-exposed eye and naïve controls.[8] In the D2 eye, corneal edema occurred in 52% of eyes at 3 days dpi (n = 27) and remained in 43% of mice at 28 dpi (n = 7, Fig 1B). Cataracts were observed in 30% of D2 eyes at both 3 and 28 dpi (Fig 1B). Pathologies that became more prevalent later included corneal neovascularization and corneal calcifications. Corneal neovascularization was detected in 44% and 29% of eyes at 14 (n = 9) and 28 dpi, respectively (Fig 1D and 1E). Corneal calcification was detected in 33% and 43% of eyes at 14 and 28 dpi, respectively (Fig 1E). Note that calcium deposits in the cornea were present in many of the D2 blast and naïve control mice as a normal finding for this strain (Fig 1C and 1D) [15]. Similar to our previous results in the blast-exposed eye, treatment with non-medicated eye drops prevented all of the corneal pathology. Thus, we treated all following mice with non-medicated eye drops to prevent corneal pathology, unless otherwise stated in order to test visual function.

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