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Updated: Jul 5, 2026
A Murine Model of Ischemic Retinal Injury Induced by Transient Bilateral Common Carotid Artery Occlusion
Published on: November 12, 2020
Filamentous middle cerebral artery occlusion causes ischemic damage to the retina in mice
Ernest C Steele1, Qingmin Guo, Shobu Namura
1Department of Anatomy and Neurobiology, Morehouse School of Medicine, 720 Westview Dr SW, Atlanta, GA 30310, USA.
Background And Purpose:
Filamentous middle cerebral artery occlusion (fMCAO) is the most frequently used focal cerebral ischemia model in rodents. The proximity of the ophthalmic artery to the middle cerebral artery suggests that fMCAO induces retinal ischemia. We therefore tested whether fMCAO induces ischemia/reperfusion damage in retina in mice.
Methods:
SV129EV mice were subjected to transient (30 or 60 minutes) fMCAO followed by reperfusion under isoflurane anesthesia. Retinal perfusion was evaluated by intravenous injection of fluorescent microspheres combined with fluorescent microscopy using flat-mounted retinas. The fluorescent density of ipsilateral retina relative to contralateral retina was determined in each animal. Retinal injury was assessed by cresyl violet staining and in situ TUNEL.
Results:
Microsphere analysis demonstrated perfusion defect in the ipsilateral retina after 60 minutes fMCAO and effective restoration after reperfusion. Thirty minutes fMCAO did not produce evident histological changes, even after 2 days of reperfusion. Sixty minutes fMCAO followed by 2 hours reperfusion resulted in extensive cell damage in the inner nuclear (>30%) and ganglion cell (>50%) layers. TUNEL demonstrated very few positive cells, suggesting that damaged cells were mainly undergoing nonapoptotic cell death.
Conclusions:
Sixty minutes fMCAO produces retinal injury in SV129EV mice. Potential visual dysfunction should be considered when a particular occlusion period is selected for studying neurological outcomes after fMCAO. Because visual disturbance is often associated with thrombotic/embolic stroke in humans, fMCAO represents an appropriate model for future studies aimed at understanding and ameliorating the changes that lead to retinal damage in these patients.
Insights
Filamentous middle cerebral artery occlusion (fMCAO) in mice causes retinal ischemia and cell damage, particularly after 60 minutes. This finding is crucial for understanding stroke-related visual dysfunction.
Area of Science:
- Neuroscience
- Ophthalmology
- Ischemia Research
Background:
- Filamentous middle cerebral artery occlusion (fMCAO) is a common rodent model for focal cerebral ischemia.
- The anatomical proximity of the ophthalmic artery to the middle cerebral artery suggests potential retinal ischemia during fMCAO.
Purpose of the Study:
- To investigate whether fMCAO induces ischemia/reperfusion damage in the retina of mice.
- To evaluate the impact of different occlusion durations on retinal injury.
Main Methods:
- Transient fMCAO (30 or 60 minutes) was performed on SV129EV mice.
- Retinal perfusion was assessed using fluorescent microspheres and microscopy.
- Retinal injury was evaluated via cresyl violet staining and TUNEL assays.
Main Results:
- Sixty minutes of fMCAO caused significant retinal perfusion defects, with recovery after reperfusion.
- Extensive cell damage occurred in the inner nuclear and ganglion cell layers after 60 minutes of fMCAO and 2 hours of reperfusion.
- Thirty minutes of fMCAO did not result in significant histological changes.
Conclusions:
- A 60-minute fMCAO model in mice induces retinal injury and cell death, primarily non-apoptotic.
- Potential visual dysfunction must be considered when using fMCAO for neurological outcome studies.
- fMCAO serves as a relevant model for studying retinal damage in human thrombotic/embolic stroke.
