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A ctivation of NMDA receptors and L-type voltage-gated calcium channels mediates enhanced formation of Fyn-PSD95-NR2A complex after transient brain ischemia
Brain Research 1955(2002)123-132,-0001,():
Recent studies have indicated that tyrosine phosphorylation of NMDA receptor subunit 2A (NR2A) by Src family kinases (Src, Fynetc.) up-regulates NMDA receptors activity and postsynaptic density protein 95kDa (PSD95) may mediate the regulation. To investigatewhether the above processes are involved in brain ischemia-induced enhancement of NMDA receptors function, we examined the effectsof transient (15min) brain ischemia followed by reperfusion on interactions involving Fyn, NR2A and PSD95 in rat hippocampus byco-immunoprecipitation. Transient brain ischemia was induced by the method of four-vessel occlusion in Sprague-Dawley rats.Association between Fyn and NR2A increased immediately after brain ischemia and the increase was maintained for at least 24h duringfollowed reperfusion, up to about 1.7-1.8-fold relative to sham-groups. The 15min reperfusion after brain is hemia induced enhancedco-immunoprecipitation of PSD95, Fyn and NR2A with one another. The associations of PSD95 with Fyn and NR2A increased at 0-24h, 0-1h of reperfusion, up to 6.9- and 2.1-fold relative to sham groups, respectively. Inhibiting activation of NMDA receptors or L-typevoltage-gated calcium channels (L-VGCC) by ketamine or nifedipine attenuated the above increases of associations. These results suggestthat stimulation of NMDA receptors and L-VGCC facilitates formation of a ternary complex: Fyn-PSD95-NR2A during transient brainischemia followed by reperfusion, which may result in potentiation of NMDA receptor function and contribute to ischemic neuronal cell death.
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