We have employed paired associative transcranial magnetic stimulation (PAS), or theta-burst transcranial magnetic stimulation (TBS) for induction of long-term potentiation (LTP)-like and long-term depression (LTD)-like plasticity in human motor cortex, as indicated by lasting increases/decreases in motor evoked potential amplitudes. In a first set of experiments we demonstrated that practice of simple ballistic finger movements, leading to improved peak acceleration (i.e. kinematic motor learning) of the trained movement, resulted in abolition of subsequent PAS-induced LTP-like plasticity but enhancement of LTD-like plasticity (Ziemann et al., 2004). These interactions strongly suggested that PAS-induced plasticity and kinematic motor learning share common mechanisms. In a next step, using PAS-induced plasticity as a surrogate marker for motor learning, we demonstrated that priming with another PAS protocol resulted in homeostatic or non-homeostatic regulation of the subsequent PAS-induced plasticity, depending on the interval between the two protocols (Müller-Dahlhaus et al., in preparation). In additional TBS experiments, we showed that plasticity of inhibitory circuits, as tested by paired-pulse transcranial magnetic stimulation are regulated by homeostatic metaplasticity (Murakami et al., 2012). In a third step, we demonstrated that kinematic motor learning is regulated by homeostatic or non-homeostatic metaplasticity when primed by PAS-induced LTP- or LTD-like plasticity, depending on the interval between priming PAS and kinematic motor learning (Jung & Ziemann, 2009). These data are rather important because they suggest that priming of motor learning by non-invasive brain stimulation may be utilized to enhance learning success. Finally, we showed absent regulation of kinematic motor learning by preceding PAS in patients with task-dependent hand dystonia (writer’s cramp), with the magnitude of this abnormality correlating to the clinical severity of dystonia (Kang et al., 2011). Therefore, testing the interaction between brain stimulation and motor learning may contribute to our understanding of the pathophysiology of movement disorders and may also be used for diagnostic purposes.