TDCS modulates the excitability of a targeted brain region non-invasively by altering neuronal membrane potentials (Bindman et al. 1962; Purpura & McMurtry, 1965). Thus, this technique can be used to increase or decrease the excitability of neurons in a targeted brain area and this can establish a causal relation between a given region of the brain and a specific sensory, motor or cognitive function. Unlike Transcranial Magnetic Stimulation (TMS), TDCS does not depolarize neurons causing them to fire. TDCS only alters the likelihood that neurons will fire by depolarizing or hyperpolarizing brain tissue (depending on the stimulation parameters used). The neurophysiological basis of TDCS has been attributed to a mechanism akin to long-term potentiation (LTP) and long-term depression (LTD) (Hattori et al. 1990; Moriwaki, 1991; Islam et al. 1995). Certain medications such as dextromethorphan (an NMDA antagonist) suppress post-TDCS stimulation effects of both anodal and cathodal stimulation which strongly suggests the involvement of NMDA receptors in both types of DC-induced neuroplasticity. In contrast, Carbamazepine selectively eliminates anodal effects. Since Carbamazepine stabilizes the membrane potential voltage-dependently, the results reveal that after-effects of anodal TDCS require a depolarization of membrane potentials (Liebetanz et al., 2002). This study by Liebetanz et al., (2002) provided pharmacological evidence that induction of the after-effects of TDCS requires a combination of glutamatergic (excitatory) and membrane mechanisms, similar to the induction of established types of short- or long-term neuroplasticity.