Figure 2.

ECT effects on neurotransmitters. ECT has a variety of effects on important neurotransmitters and/or their receptors. These include (A) the ECT noradrenergic effect that decreases the α2 adrenergic receptors’ affinity to their ligands, noradrenaline. Likewise, ECT has glutaminergic effects that could be generated through some of the following pathways: (B) a decreases in the glutamate concentration after ECT with a consequent increase in neurogenesis or (C) an increase in the glutamate concentration after ECT, which is associated not only with the neuroinflammation but also with the promotion of angiogenesis, which is part of neurogenesis. Regardless, (D) another effect of ECT involves GABA because the levels of this neurotransmitter increase after ECT. Furthermore, ECT generates changes in the dopaminergic receptor family, such as (E) a decrease in the affinity of the D2 receptor to its ligand [(11)C]FLB 457 radioactive, and (F) ECT increases protein synthesis and the gene expression codifying for the D1 receptor. It also improves the D1 receptors’ affinity to their ligands. Finally, (G) this therapy has effects on the serotoninergic systems and BDNF through an increase in the serotonin levels, which promotes neuroplasticity through the BDNF synthesis stimulation. However, ECT also causes an increase in the proBDNF levels, which promotes neuronal apoptosis and has antiplasticity effects, which makes the tPA role a crucial one as it is an important element in the transformation from proBDNF to mBDNF. The latter is the one responsible for the neuroplasticity promotion. ECT: electroconvulsive therapy; BDNF: brain-derived neurotrophic factor; proBDNF: precursor isoform of BDNF; tPA: tissue plasminogen activator.