Neuroplasticity represents the dynamic structural and functional reorganization of the central nervous system, including its connectivity, due to environmental and internal demands. It is recognized as a major physiological basis for adaption of cognition and behaviour, and, thus, of utmost importance for normal brain function. Cognitive dysfunctions are major symptoms in psychiatric disorders, which are often associated with pathological alteration of neuroplasticity. Transcranial direct current stimulation (tDCS), a recently developed non-invasive brain stimulation technique, is able to induce and modulate cortical plasticity in humans via the application of relatively weak current through the scalp of the head. It has the potential to alter pathological plasticity and restore dysfunctional cognitions in psychiatric diseases. In the last decades, its efficacy to treat psychiatric disorders has been explored increasingly. This review will give an overview of pathological alterations of plasticity in psychiatric diseases, gather clinical studies involving tDCS to ameliorate symptoms, and discuss future directions of application, with an emphasis on optimizing stimulation effects.

Dopamine plays an important role in the modulation of neuroplasticity, which serves as the physiological basis of cognition. The physiological effects of dopamine depend on receptor subtypes, and the D1 receptor is critically involved in learning and memory formation. Evidence from both animal and human studies shows a dose-dependent impact of D1 activity on performance. However, the direct association between physiology and behavior in humans remains unclear. In this study, four groups of healthy participants were recruited, and each group received placebo or medication inducing a low, medium, or high amount of D1 activation via the combination of levodopa and a D2 antagonist. After medication, fMRI was conducted during a visuomotor learning task. The behavioral results revealed an inverted U-shaped effect of D1 activation on task performance, where medium-dose D1 activation led to superior learning effects, as compared to placebo as well as low- and high-dose groups. A respective dose-dependent D1 modulation was also observed for cortical activity revealed by fMRI. Further analysis demonstrated a positive correlation between task performance and cortical activation at the left primary motor cortex. Our results indicate a nonlinear curve of D1 modulation on motor learning in humans and the respective physiological correlates in corresponding brain areas.

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Background Noradrenaline (NA) has an important role as a neuromodulator of the central nervous system. Noradrenergic enhancement was recently shown to enhance glutamate-dependent cortical facilitation, and long term potentiation-like plasticity. As cortical excitability and plasticity are closely linked to various cognitive processes, here we aimed to explore whether these alterations are associated with respective cognitive performance changes. Specifically, we assessed the impact of noradrenergic enhancement on motor learning (serial reaction time task), attentional processes (stroop interference task), and working memory performance (n-back letter task). Methods The study was conducted in a cross-over design. Twenty-five healthy humans performed the respective cognitive tasks after a single dose of the noradrenaline reuptake inhibitor reboxetine (RBX) or placebo (PLC) administration. Results The results show that motor learning, attentional processes, and working memory performance in healthy subjects were improved by RBX application, as compared to PLC. Conclusions The results of the present study thus suggest that noradrenergic enhancement can improve memory formation and executive functions in healthy humans. The respective changes go in line with related effects of noradrenaline on cortical excitability and plasticity.