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However, it has yet to be determined whether EDA can attenuate iodoacetic acid- (IAA-) induced neuronal death<jats:italic>in vitro<\/jats:italic>. In the present study, we investigated the effect of EDA on damage of IAA-induced primary cerebellar granule neurons (CGNs) and its possible underlying mechanisms. We found that EDA attenuated IAA-induced cell injury in CGNs. Moreover, EDA significantly reduced intracellular reactive oxidative stress production, loss of mitochondrial membrane potential, and caspase 3 activity induced by IAA. 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