Metal Toxicity at the Synapse: Presynaptic, Postsynaptic, and Long-Term Effects

Figure 1

Presynaptic targets of neurotoxic metals. Events at the synapse from the arrival of the action potential which results in the membrane depolarization-induced opening of voltage-activated calcium channels and the entry of calcium which activates CaM, which activates CaM kinases and causes the phosphorylation of synaptic vesicle-associated proteins and an increase in readily releasable neurotransmitter vesicles. Calcium also binds synaptotagmin and causes exocytosis of neurotransmitter from the vesicles. Shown in boxes are the metals and the targets at which they act in the synaptic transduction pathway. A table at the end indicates the symbols and what they indicate. Green indicates activation or upregulation while red indicates inhibition or downregulation. Please refer to the section of Abbreviations and metals.