Metabolic modulation of neuronal excitability is becoming increasingly important as an antiepileptic therapy.It was reported that the glycolytic inhibitor 2-deoxy-D-glucose (2-DG) and the activation of the ATP-sensitive potassium ion channel (KATP channel) had an antiepileptic effect in models of epilepsy.To explore whether 2-DG exerts an antiepileptic effect through upregulation of the KATP channel subunits Kirr.1 and Kirr.2, the expression of these subunits in hippocampus of five groups of mice with pilocarpine-induced status epilepticus (SE) was evaluated.A seizure group with pilocarpinekindling convulsions (EP) was compared to similar groups treated with high, medium, and low 2-DG concentrations (100-500mg/kg) and a normal control group (Con).Kir6.1 and Kir6.2mRNAs and proteins were analyzed at 4 h, 1 d (acute period),7 d (latent period), 30 d, and 60 d (chronic period) following SE.In the seizure group (compared to the Con group),hippocampal expression of Kir6.1 and Kir6.2 increased dramatically at 1 d, 7 d, and 30 d, and was further increased after treatment with medium and high dose 2-DG (all P<0.05).Our results suggest that 2-DG may exert an antiepileptic effect through up-regulation of mRNAs and protein levels of Kir6.1and Kir6.2, which may therefore be used as molecular targets in the treatment of epilepsy with 2-DG.