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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   [ C a 2 + ] 𝑚 .