The effects of glutamate transporters on synaptic plasticity in rat models of pilocarpine-induced status epilepticus were investigated. Male Wista rats ((304.06±13.79) g) were randomly divided into 5 groups, short-term seizures (SE) and its control (SC), long-term seizures (LE) and its control(LC), normal control (Sham) groups. Epilepsy rat models were induced by injection of pilocarpine(25 mg/kg, i.d.). Glutamate transporter inhibitor, DL-threo-benzyloxyaspartate (TBOA, 7.5 nmol，1 μl) was microinjected into right side of hippocampus after 14 days of initial status epilepticus in SE and LE groups. The same volumes of artificial cerebrospinal fluid were injected into same side of hippocampus in SC and LC groups. Electroencephalographys (EEG) were detected in SE and SC groups after 2 h of drug injection. Long term potential (LTP) at perforant pathway and dentate gyrus(PP-DG) and EEG were recorded in LE and LC groups after two weeks of drug injection. Example of Fluoro-Jade-B staining in the rat brain was made at the end of electrophysiological experiment. The results showed that there was a significant decrease in theta band power of EEG in SE group compared with that of SC group (P < 0.05). There was no significant difference in theta band power of EEG between LE and LC groups(P > 0.05). The slope of excitatory postsynaptic potential (EPSP) was significantly increased in LE group compared with that of LC group (P < 0.01). Fluoro-Jade-B showed more neuronal degeneration in LE group compared with that of LC group. The results suggested that TBOA induced damage of glutamate transporters and enhanced the neurotoxicity of status epilepticus, which contributed the synaptic plasticity in status epilepticus rats.