The major findings of this study are that the KCa3.1 channel contributes to reactive astrogliosis following ischemia, as shown in both OGD-treated astrocytes in vitro and the brains of mice subject to pMCAO in vivo, that KCa3.1 regulated Ca2+ influx and membrane potential by functional cooperation with the TRPV4 channel in OGD-treated astrocytes. Here, KCNN4 is linked to ischemia.