Hypoxic-ischemic retinal injury in rat pups.
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.


CONCLUSIONS
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.
Department of Ophthamology, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Hsiu-Mei
HM
Huang
Chao-Ching
CC
Huang
Pi-Lien
PL
Hung
Ying-Chao
YC
Chang
D000818:Animals; D017209:Apoptosis; D016923:Cell Death; D004596:Electroretinography; D000860:Hypoxia / Q000150:complications*; D007511:Ischemia / Q000150:complications*; D009474:Neurons / Q000473:pathology; D051381:Rats; D012160:Retina / Q000293:injuries* / Q000473:pathology