Abstract
One of the pathophysiologies of depression is the neuroplasticity hypothesis, and rTMS is precisely a physical therapy that exerts its therapeutic effects by neuromodulating the neuroplasticity of brain networks. Previous studies have suggested that GABA, NMDA, AMPA, and BDNF are involved in the therapeutic mechanism of rTMS at the molecular level. At the neuroimaging level, functional connectivity between the DLPFC and subgenual anterior cingulate cortex, within the default mode network and central executive network, and between the left DLPFC and striatum as measured by resting‐state functional MRI are thought to be involved. In this article, the neurobiological mechanisms of rTMS for depression, including the findings of rTMS research conducted by the author, and the future direction and prospects of rTMS are discussed.
