Delayed Oxidative Injury to the Superior Colliculus and Retinal Changes After Cerebral Hypoperfusion/Reperfusion Injury

• Main Author: Ramsaroop, Lynzey
• Other Authors: Yucel, Yeni
• Language: en_ca
• Published: 2009
• Subjects: bilateral common carotid artery occlusion; superior colliculus; nitrotyrosine; rodent; retinal ganglion cell; stroke; 0317
• Online Access: http://hdl.handle.net/1807/17441

Damage to visual pathways can lead to irreversible blindness. Posterior visual pathways, located within a watershed area, are predisposed to hypoperfusion/reperfusion injury. In a novel rat model of bilateral common carotid artery occlusion (BCCAO), oxidative injury to the superior colliculus (SC), a major visual center within the watershed area was evaluated, in addition to its effects on retinal ganglion cells (RGCs). Nitrotyrosine, a footprint of peroxynitrite-mediated oxidative injury in the SC, and microtubule-associated protein 2, a dendrite marker in the retina, were assessed using immunofluorescence and confocal microscopy. Nitrotyrosine-immunoreactivity in the SC was increased 2 weeks after BCCAO compared to controls. Microtubule-associated protein 2-immunoreactivity in the central inner plexiform layer was reduced 3 weeks after BCCAO compared to controls. Global incomplete cerebral hypoperfusion/reperfusion induced oxidative injury in the SC and retrograde RGC dendritic changes. This suggests that cerebrovascular injury affecting the posterior visual pathways may contribute to vision loss in patients.