Additionally, 17β-estradiol can activate estrogen receptors to lower the excitotoxicity in ischemia by potentiating the activity of BK channels and decreasing the AMPA/NMDA receptor-mediated spontaneous excitatory postsynaptic currents (sEPSCs), a process that is indicative of the interplay between BK and other ion channels in estrogen-induced neuroprotection (Zhang et al., 2009). Here, KCNMA1 is linked to ischemia.