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Our previous study showed that propofol (20 mg · kg-1 · h-1) postconditioning explored long term (up to 28 days) neuroprotection to cerebral ischemia/reperfusion injury.1 However, the mechanism of such effect induced by propofol postconditioning largely remains elusive.α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) mediate fast synaptic transmission at excitatory synapses in the central nervous system (CNS) and AMPARs-mediated excitotoxicity is thought to play a critical role in CNS ischemic insults.2,3 We here investigated role of AMPA receptor GluR1 subunit trafficking during propofol postconditioning.