Time course of brain damage and expression of related molecules in rats with transient global cerebral ischemia

Objective: To investigate the time course of brain damage and the expression of related molecules during reperfusion after transient global cerebral ischemia in rats. Methods: Brain damage was induced by four vessel occlusion (4VO). After 1 14 days brain pathological changes were observed and expression of N methyl D aspartate(NMDA) receptor subunits and vascular cell adhesion molecule 1(VCAM 1) molecules in the cortex and hippocampus was measured by immunoblotting. Results: Three to fourteen days post 4VO induced global cerebral ischemia, the hippocampal CA1 region showed the delayed neuronal death. The expression of NMDA receptor su bunit 1 (NR1) and NMDA receptor subunit 2A (NR2A) in the cortex increased by the first and third day respectively; NMDA receptor subunit 2B (NR2B) expression showed high level on 1st and 3rd days. In the hippocampus, NR1 subunit expression decreased on day 1, but gradually increased thereafter and reached a peak level by the 14th day; NR2A and NR2B subunits expression similarly increased by the 7th day. VCAM 1 expression in the hippocampus and cortex increased by the 3rd and 7th days respectively. Conclusion: During reperfusion after transient global cerebral ischemia, hippocampal neuron density decreases. Peak expression of NMDA receptor subunits (NR1? NR2A?NR2B) and VCAM 1 molecules occurs according to a different time course specific to brain area, cortex vs. hippocampus. Interfering their expression may attenuate cerebral ischemia/reperfusion induced neural damage.