Background: T-type calcium (Cav3.2) channel inhibitors prevent neuronal death during ischemia,but the cytotoxic signals have not been resolved. Results: Cav3.2 channels generate cytotoxic calcium elevations in the cytosol and mitochondria of PC12 cells deprived of oxygen and glucose. Conclusion: calcium transfer from Cav3.2 channels to mitochondria contributes to ischemic toxicity Significance: Cav3.2 channels and the mitochondrial calcium uniporter (MCU) are potential targets for the treatment of stroke.