Figure 5.

M1, Primary motor cortex; DLPFC, dorsolateral prefrontal cortex; S1, primary somatosensory cortex; S2, secondary somatosensory cortex; PFC, prefrontal cortex; ACC, anterior cingulate cortex; PCC, posterior cingulate cortex; INS, Insula; TH–VPL, thalamus-ventral posterolateral nucleus; TH-MD, thalamus-medial dorsal nucleus; HT, hypothalamus; AMY, Amygdala; PAG, periaqueductal gray matter;RVM, rostral ventromedial medulla; NMDAR, N-methyl-D-aspartate receptor; AMPAR, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor; Trk, Tropomyosin receptor kinase; Ca²⁺, calcium; K⁺, potassium; Na⁺, sodium; Mg², magnesium; +, excitatory; -, inhibitory; L-LTP, late long-term potentiation. (1) The anodal tDCS increases the intracellular Ca²⁺ flow that releases more neurotransmitters. (2) The positive regulation of neurotransmitters facilitates the openness of AMPA channels and indirectly of NMDA channels, which characterizes the long-term potentiation (LTP). (3) Activation of tropomyosin receptor (Trk) indicates the role of brain-derived neurotrophic factor (BDNF) in the anodal tDCS; its effect increases the production of the synaptic vesicles and the neurotransmitter release. (4) Increase of Ca²⁺ flow promotes the release of neurotrophic factors for the synaptic cleft. (5) Post-synaptic Trk receptor induces the late LTP (L-LTP) and favors the openness of the NMDA channels, which reinforces the L-LTP. (6) Both L-LTP and L-LTD are highly dependent on the modification of gene expression.