Objective To investigate the variations of ionotropic glutamate receptors mediating epileptiform activity in rat hippocampal CAI region in order to explore the mechanism of epileptogenesis. Methods The epileptiform activity was induced by perfusing normal hippocampal slices with GABAA receptor antagonist bicuculline ( 30 μmol/L ) and temporal lobe epilepsy ( TLE ) model was established by kainic acid( KA ) injected into the CA3 region of the right hippocampus. The population spike ( PS ) of CAI pyramidal cells was recorded with extracellular recording in hippocampal slices by electrical stimulating Schaffer collateral in stratum radiatum. Results Single PS , which mainly mediated by non-NMDA receptors, was recorded in normal hippocampal slices. The multiple epileptiform discharges, which partially mediated by NMDA receptor in addition to non-NMDA receptors, could be induced by perfusing bicuculline. After perfusing NMDA receptor antagonist, APV ( 50 μmol/L ), the amplitude of the first PS was not significantly affected , however , the amplitude offourth and fifth PS was decreased obviouslv( n = 11 , P ＜ 0 . 0 5 ;n = 9 ,P 0.05),而第4和第5个PS幅度明显降低 (n=11,P0.05),第4和第5个PS幅度明显降低(n=8,P<0.05; n=8,P<0.01),并可进一步抑制灌流非NMDA受体拮抗剂6-氰基-7-硝基喹噁啉-2,3-土卫四(CNQX) (10 μmol/L)后的残留电位.结论 大鼠海马CA1区NMDA受体的激活参与癫痫样活动的发生.
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