Objective The epileptiform activity was induced by perfusing GABAA receptor antagonist bicuculline (Bic, 30 μmol/L) in normal hippocampal slices and temporal lobe epilepsy (TLE) model was established by kainic acid (KA) injected into the center site of right hippocampus CA3 region with the stereotaxic technology.To investigate the variations of ionotropic glutamate receptors mediating epileptiform activity in rat hippocampal CA1 region by using extracellular recording in hippocampal slices, and to explore the mechanism of epileptogenesis.Methods Population spike (PS) was recorded in CA1 pyramidal cell layer by stimulating the Shaffer collaterals in stratum radiatum using extracellular field-potential recording.Results (1) Single PS was usually recorded in normal pyramidal cell layer of hippocampal CA1 region.Perfusing normal hippocampal slices with Bic (30 μmol/L) could induce multiple epileptiform discharges, in which the PS number was (5.07 ± 0.30, n =11), the amplitude of the first PS was increased significantly by (150.86 ± 22.56) % (n =11, P < 0.01) compared with the control.Epileptiform discharges could recorded in slices of TLE model rats, the PS number was (6.12 ± 0.33, n =9).The PS number was increased significantly in slices of epileptiform activity compared with the control (P < 0.01).(2) Variations of ionotropic glutamate receptors mediating PS in hippocampal CA1 region.The PS recorded in normal pyramidal cell layer ofhippocampal CA1 mainly mediated by non-NMDA receptors.The PS recorded in normal slices after perfusing with Bic was partially mediated by NMDA receptor in addition to non-NMDA receptors.After perfusing with NMDA receptor antagonist, APV (50 μmol/L), the amplitude of the first PS was not significantly affected (n =11, P > 0.05), however, the amplitude of the fourth and fifth PS was decreased obviously (n =11, P < 0.05; n =9, P < 0.05).After perfusing APV in slices of TLE model rats, the amplitude of the first PS was not significantly affected (n =9, P > 0.05), but the amplitude of the fourth and fifth PS was decreased obviously (n =8, P < 0.05; n =8, P < 0.01), moreover, APV could inhibit the residual potential after perfusing non-NMDA receptor antagonist, CNQX (10 μmol/L).Conclusion (1) Both slices of normal rats perfused with Bic and slices of TLE model rats could induce epileptiform activity, and increased the PS number in CA1 region.(2) In addition to non-NMDA receptors, the activation of NMDA receptor contributes to epileptiform activity in hippoeampal CA1 region.