Fig. 3

Diagram illustrates the observed effects of Sal-induced toxicity in DRGNs. Sal triggers an increase of cytosolic Na⁺ concentrations, with a secondary increase in cytosolic Ca²⁺, which is mediated by NCXs in the plasma membrane and mitochondria. Elevatory intracellular Ca²⁺ levels activate the protease calpain, which leads to apoptotic cell death by the activation of caspase pathways involving caspase 12, caspase 9 and caspase 3. Caspase 9 can be alternatively activated by cytochrome c released from depolarized mitochondria