## 3 Brain Stimulation Techniques
### The Effect of tDCS and tMS on Neuroplasticity  
Neuroplasticity is a broad term that describes the brain's ability to adapt and learn through cellular and molecular changes in neurons, resulting in alterations to both the activity and structure of neural networks. Synaptic plasticity involves synaptogenesis, the formation and organization of new synapses, while non-synaptic plasticity refers to processes like neuronal migration and neurogenesis. These changes can be detected through brain imaging, which reveals lasting alterations in regional neural function or neuroanatomy [40]. [PERSON] et al. [41] reported that tDCS could also be used as a tool for neuroenhancement in terms of cognitive functions such as working memory. This is a highly relevant aspect as studies have reported that cognitive reserves play the role of an important neuroprotective factor in mood disorders such as depression [42]. Additionally, [PERSON] et al. [43] found that cognitive dysfunction is a core symptom of MDD, so the use of tDCS as a neuroenhancer could potentiate the internal physiological mechanisms as a symptom-oriented therapy.  
The neurophysiological effects of tDCS typically extend beyond the immediate stimulation period [31]. Long-term potentiation (LTP), which refers to the enduring enhancement of synaptic transmission and serves as the cellular basis for learning and memory, was first observed in hippocampal neurons [44]. Both cortical LTP and long-term depression (LTD) are influenced by glutamatergic and GABAergic neurons [45]. Enhanced excitability induced by anodal tDCS in the primary motor cortex resembles LTP and is dependent on the activity of N-methyl-D-aspartate (NMDA) receptors and calcium channels [46]. The strength, duration, and direction of stimulation nonlinearly affect whether excitatory or inhibitory effects are produced [46].  
Neuroplasticity, often associated with rehabilitation following brain injury, is also recognized as a key mechanism in treatments such as antidepressants, psychotherapy, and attention-based interventions [47]. Neuroimaging studies have revealed changes in brain function, with tDCS being shown to modulate distinct resting-state networks as observed through functional magnetic resonance imaging (fMRI) [48]. Specifically, active anodal tDCS applied to the left dorsolateral prefrontal cortex led to significant alterations in connectivity within the default network, self-referential network, and frontal-parietal networks when compared to placebo tDCS interventions. Evidence suggests that the blockade of voltage-gated sodium and calcium channels reduces the effect of anodal tDCS on increasing excitability. In contrast, the reduction in excitability produced by cathodal tDCS is unaffected. These findings are consistent with the assumption that tDCS induces changes in the resting membrane potential of cortical neurons [49].  
Among the physiological explanations describing the effects of tDCS, an interesting theory explains the impact of weak currents acting through a stochastic and rhythmic resonance that influences neural information encoding [50]. More precisely, it was suggested that the occurrence of small changes in spike predictability and timing would subtly influence cognition through neural population coding [51], which is further linked to the neuroplasticity mechanism [52].  
Traditional tMS has been used primarily on the motor cortex as a target for investigating mechanisms of plasticity, such as LTP and LTD. Studies have focused on measuring MEPs before and after the tMS protocol.  
tMS treatment modulates neuronal activity through the interaction of glutamate, GABA, and other neuromodulators such as acetylcholine, dopamine, or serotonin. By applying a short, rapid series of electrical pulses, theta-burst stimulation (TBS) modulates synaptic efficiency, either strengthening it (by intermittent TBS-iTBS) or weakening it by continuous TBS-cTBS.