Expression Of MAP2, GAP-43 And Synaptophysin In Chronic Cerebral Ischemia Rats Hippocampus And Its Relation With Cognitive Impairment

Objective : To investigate mRNA and protein expression of MAP2, GAP-43 and synaptophysin in the hippocampus of Wistar rats after chronic cerebral ischemia and its relation with cognitive impairment.Methods: Chronic cerebral ischemia was induced by permanent occlusion of bilateral common carotid arteries (2-VO) in male Wistar rats. Rats were assigned to 4 groups: those with chronic cerebral ischemia for 4, 10, 20 weeks and those given sham operation. Learning and memory performance were examined in rats using a Morris water maze task. MAP-2, GAP-43 and synaptophysin protein and mRNA levels of 4 groups were measured using Western Blotting and SYBR Green real-time RT-PCR respectively. A correlation analysis was made between mRNA and protein expression of MAP-2, GAP-43 and synaptophysin in the hippocampus of Wistar ratsand Learning and memory performance in Morris water maze task.Results: The learning and memory performance were gradually impaired in the chronic cerebral ischemia rats with the increase of ischemia duration. In the 2-VO 4 weeks rats synaptophysin protein levels were down-regulated in the hippocampus compared to the sham operation rats(P<0.05); in the 2-VO 10 weeks rats synaptophysin protein(P<0.01) and MAP2 protein(P<0.05) levels were down-regulated in the hippocampus compared to the sham operation rats; in the 2-VO 20 weeks rats synaptophysin protein, MAP2 protein and mRNA levels were significantly down-regulated in the hippocampus compared to the sham operation rats(P<0.01). synaptophysin protein, MAP-2 protein and mRNA levels are positively correlate with learning and memory performance in Morris water maze task.Conclusion: These results indicate that chronic cerebral ischemia induce down-regulate of synaptophysin protein, MAP-2 protein and mRNA in thehippocampus of permanent 2-VO rats, which is closely relates with learning and memory performance and may be molecular mechanism of impaired learning and memory after chronic cerebral ischemia.