Abstract
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. 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. 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. 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.
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