Objective: To investigate the effects of TCA on neuroinflammation and excitotoxicity induced by global cerebral ischemia(GCI)and the mechanisms of improving the impairment of memory and synaptic plasticity.Methods: Global cerebral ischemia model were established according to the method of four-vessel occlusion.SD rats were randomly divided into four groups: Sham,Sham+TCA,GCI and GCI+TCA.Sham+TCA and GCI+TCA group were pretreated with the feed containing TCA(240ppm)for 28 d,and then,GCI model was established.After 7 days recovery,to determinate cognition and motor function,rats in four groups were carried out the following behavioral tests: open field,novel object recognition task and Morris water maze.Immunofluorescence staining,Nissl staining and Western blot were used to observe the protective effects of TCA on the damage of hippocampal CA1 pyramidal neurons and the expression of iNOS,COX-2,NR2B and p-αCaMKII in CA1 area of hippocampus following GCI.Electrophysiological recording in vivo was analyzed change of basal synaptic function、neurotransmitter release function of presynapticity and long term potentiation(LTP)on CA1-Schaffer collateral commissural pathway.Results: The results of behavioral tests indicate that TCA significantly lessened memory deficit without the change of locomotor activity and nervous-like behavior following GCI.TCA inhibited microglial activation and neuronal damage,and expression of iNOS and COX-2 in hippocampal CA1 area after GCI,suggesting that TCA may exert neuroprotective effect through inhibition of neuroinflammation following GCI.After electrophysiological recording in vivo,the results indicate that TCA did not affect presynaptic release of neurotransmitter function in rats,but significantly improved GCI-induced LTP inhibition in CA1-Schaffer collateral commissural pathway.TCA can inhibit the increase of NR2B and p-αCaMKII expression after GCI,suggesting that TCA may reduce the excitotoxity induced with neuroinflammation.Conclusions: This study demonstrates that TCA improved memory deficit and synaptic plasticity damage and suppressed microglia activation by inhibiting neuroinflammation and excitoxity induced by global cerebral ischemia.