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Updated: May 21, 2026
Oxygen-Induced Retinopathy Model for Ischemic Retinal Diseases in Rodents
Published on: September 16, 2020
Hypoxic-ischemic retinal injury in rat pups
Hsiu-Mei Huang1, Chao-Ching Huang, Pi-Lien Hung
1Department of Ophthamology, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Insights
Hypoxic-ischemic (HI) insults cause significant, long-term damage to the retinas of immature rats, affecting vision. This study provides the first evidence of HI-induced retinal damage in neonatal rats, highlighting the need for neuroprotective strategies.
Area of Science:
- Neuroscience
- Ophthalmology
- Pediatric Neurology
Background:
- Visual impairment in children is often linked to brain damage, particularly hypoxic-ischemic (HI) encephalopathy.
- HI insults are hypothesized to inflict long-term damage on developing eyes.
Purpose of the Study:
- To investigate the long-term effects of HI insults on immature rat retinas.
- To establish evidence of HI-induced retinal damage at pathological and functional levels.
Main Methods:
- HI was induced in postnatal day 7 rat pups via carotid artery ligation and hypoxia.
- Retinal damage was assessed using electroretinography (ERG), cell counting, and immunostaining for neuronal injury and astrogliosis.
Main Results:
- HI injury led to extensive, persistent damage in the retinal ganglion cell layer (GCL), inner plexiform layer, and inner nuclear layer (INL).
- Significant alterations in ERG, microglial and Müller cell activation, and apoptotic neuronal death via caspase-dependent pathways were observed.
Conclusions:
- This study presents the first evidence of HI-induced retinal damage in neonatal rats using the Vannucci model.
- Demonstrating retinal preservation is crucial when evaluating neuroprotective strategies for HI injury.
Background:
Visual loss associated with brain damage, especially hypoxic-ischemic (HI) encephalopathy, is the most common cause of visual impairment in children in developed countries. We hypothesized that HI insults can cause long-term damage in immature eyes.
Methods:
In postnatal day 7 rat pups, HI was induced by unilateral common carotid artery ligation followed by hypoxia. Retina damage was assessed by electroretinography (ERG) and cell counting. Neuronal injury and astrogliosis were evaluated by terminal deoxynucleotidyl transferase nick-end labeling, cleaved caspase 3, ED1, and glial fibrillary acidic protein immunostaining.
Results:
We observed rapid and persistently extensive injuries in the ganglia cell layer (GCL), inner plexiform layer, and inner nuclear layer (INL) in ipsilateral retinas after HI injury, corresponding to the marked alteration in ERG. HI insult caused prominent microglial and Műller cell activation in ipsilateral inner retinas. Neuronal death in the GCL and INL after HI injury was mainly apoptotic, involving caspase-dependent pathways.
Conclusion:
Our study demonstrated the first evidence of HI retinal damage at both the pathological and functional level using the Vannucci model in neonatal rats. Because retinal damage is often associated with HI injury, it is important to demonstrate that a particular neuroprotective strategy effectively preserves the retina in addition to the brain.
