Figure 1.

Schematic representation of neurobiological after-effects of transcranial electrical stimulation (tES). tES induces intracellular Ca²⁺ increase and activation of Ca²⁺-dependent enzymes (CaM-K). Presynaptic mechanisms result in glutamate release that activates AMPA/NMDA receptors, modulates BDNF release and interaction with TrkB receptor, responsible for a cascade of intracellular events that lead to de novo protein synthesis. Electrical stimulation also modulates activation of astrocytes and neuroinflammatory response. Altogether, these mechanisms may underlie the establishment of LTP/LTD. CaBP, Ca²⁺ binding proteins; CaM-K, Ca²⁺ kinases; glu, glutamate; BDNF, brain-derived neurotrophic factor; TrkB, tyrosine kinase receptor B; LTP/LTD, long term potentiation/depression; GFAP, glial fibrillary acidic protein; TNFα, tumor necrosis factor α; IL-1β, interleukin 1β; NMDAr, N-methyl-D- aspartate receptor; AMPAr, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor; GABA_A, gamma amino butirric acid A receptor.