Aim: It was generally believed that excessive potassium efflux was one of the primary causes of neuronal injury after cerebral ischemia, so inhibition of the excessive potassium channels might play a neuroprotective role.The aim of this study was to evaluate effects of potassium channel blocker tetraethylammonium (TEA) on neuronal apoptosis after oxygen-glucose deprivation (OGD) in absence or presence of astrocytes to clarify the role of the potassium channels in the cerebral ischemic injury.