In conclusion, results suggest that DEX treatment reduces cerebral ischemia-induced oxidative stress, cell death, and intracellular Ca2+ signaling through inhibition of TRPM2 and TRPV1 in the rat hippocampus and DRG;Recent studies indicate that TRPM2, a member of the TRPM subfamily of Ca(2+)-permeant, non-selective cation channel, plays an important role in mediating cellular responses to a wide range of stimuli that, under certain situations, can induce cell death. 