Aim:To determine whether ONO-1078 (pranlukast),a potent cysteinyl leukotrienereceptor 1 (CysLTI) antagonist,has an effect on N-methyl-D-aspartate (NMDA)-induced brain injury and vascular cell adhesion molecule-1 (VCAM-1) expres-sion in rats.Methods:Brain injury was induced by direct microinjection of NMDA(0.3 μmol in 1 μL of sterile 0.1 mol/L PBS,pH 7.4) into the cerebral cortex.Thelesion volume (area),brain edema and neuron density were assessed by an imageanalyzer and the expression of VCAM-1 in the cortex was detected by Westernblot 24 h after NMDA injection.ONO-1078 (0.03,0.1,or 0.3 mg/kg) andedaravone (MCI-186,10 mg/kg),a neuroprotective agent,were ip injected 30rain before and after NMDA injection.Results:NMDA microinjection producedwell-defined focal lesions (Figure 1) dose- and time-dependently.ONO-1078(0.1,0.3 mg/kg) and edaravone (10 mg/kg) decreased the total lesion volume,lesion area and brain edema induced by NMDA.Furthermore,ONO-1078 (0.1,0.3mg/kg) significantly inhibited the enhanced expression of VCAM-1 in the injuredcortices,but edaravone did not have this effect.Conclusion:CysLT_1 receptorantagonist ONO-1078 at tenufftes NMDA-induced brain damage in rats,and thismight relate to the attenuation of NMDA receptor-dependent neurotoxicity andthe inhibition of the upregulation of VCAM-1 expression. Aim: To determine whether ONO-1078 (pranlukast), a potent cysteinyl leukotriene receptor 1 (CysLTI) antagonist, has an effect on N-methyl- D-aspartate (NMDA) -induced brain injury and vascular cell adhesion molecule- 1) expres-sion in rats. Methods: Brain injury was induced by direct microinjection of NMDA (0.3 μmol in 1 μL of sterile 0.1 mol / L PBS, pH 7.4) into the cerebral cortex. The volume volume neuron density were assessed by an image analyzer and the expression of VCAM-1 in the cortex was detected by Western blot 24 h after NMDA injection. ONO-1078 (0.03, 0.1 or 0.3 mg / kg) andedaravone (MCI- kg), a neuroprotective agent, were ip injected 30 minutes before and after NMDA injection. Results: NMDA microinjection producedwell-defined focal lesions (Figure 1) dose- and time- dependently. ONO- 1078 (0.1, 0.3 mg / kg) and edaravone (10 mg / kg) decreased the total lesion volume, lesion area and brain edema induced by NMDA.Furthermore, ONO-1078 (0.1, 0.3 mg / kg) marked inhibit ed the enhanced expression of VCAM-1 in the injured cortices, but edaravone did not have this effect. Conlusion: CysLT_1 receptor antagonist ONO-1078 at tenufftes NMDA-induced brain damage in rats, and this might relate to the attenuation of NMDA receptor-dependent neurotoxicity andthe inhibition of the upregulation of VCAM-1 expression.