Role of Calcium and Mitochondria in MeHg-Mediated Cytotoxicity

Figure 4

MeHg as mediator of neuronal toxicity via Ca²⁺-mediated excitotoxicity: (1) glutamate (Glu) release from presynaptic neuron induced by MeHg; (2) increase of Glu into synaptic cleft; (3) Ca²⁺ influx via NMDA and Kainate receptors; (4) MeHg binds at Glu transporters in astrocytes; (5) mitochondria buffering the excess of Ca²⁺ intracellular; (6) MeHg causing mitochondrial and SER damage; (7) MTPT opening with release of pro-apoptotic factors induced by MeHg alone and/or excess of  [Ca²⁺]_𝑚.