Abstract: AimTo establish an in vitro model of hippocampal slice to detect electrophysiological alteration after oxygen/glucose deprivation (OGD), and to observe the effects of edaravone, minocycline and ONO-1078 pranlukast, 4-oxo-8-［P-(4-phenylbutyloxy) benzoyl-amino］-2-(tetrazol-5-yl)-4H-1-benzopyran hemihydrate. MethodsHippocampal slices from rats were perfused with artificial cerebrospinal fluid lacking oxygen and glucose for 3, 4, 7 and 10 min. The population spike (PS) was recorded, and 2,3,5-triphenyltetrazolium chloride (TTC) staining was performed in some experiments, to detect the slice viability in the presence or absence of drugs in the perfusion solution. ResultsFour min of OGD treatment was the most suitable duration for induction of slice injury, and PS amplitudes were recovered to (29±6)% of baseline values within 1 h after 4 min OGD. Edaravone, a free radical scavenger, at 1 and 10 μmol·L^-1 significantly increased the recovery rate to (56±13)% and (69±12)% of baseline respectively 1 h after OGD. However, the anti-inflammatory drug minocycline (10 μmol·L^-1) and leukotriene receptor antagonist ONO-1078 (1 μmol·L^-1) did not increase the recovery. NMDA receptor antagonist ketamine, as a positive control, also promoted the recovery concentration-dependently. ConclusionOGD for 4 min was a feasible in vitro ischemia model for determination on electrophysiological alteration in hippocampal slices. Edaravone showed concentrion-dependent protective effect on OGD injury, and anti-inflammatory drugs minocycline and ONO-1078 showed no effect.