17-β-Estradiol (E2) is a steroid hormone involved in neuroprotection against excitotoxicity and other forms of brain injury.Through genomic and non-genomic mechanisms,E2 modulates neuronal excitability and signal transmission by regulating N-methyl-D-aspartate (NMDA)and non-NMDA receptors.However,the mechanisms and identity of the receptors involved remain unclear,even though studies have suggested that estrogen G-protein-coupled receptor 30(GPR30)is linked to protection against ischemic injury.In the culture cortical neurons,treatment with E2 and the GPR30 agonist G1 for 45 min attenuated the excitotoxicity induced by NMDA exposure.