Electroconvulsive therapy (ECT) has been the most effective antidepressant treatment for over 80 years. However, its mechanism of action is still unclear. Our ECT-MRI research has revealed the following; 1) ECT induced a transient hippocampal volume increase, and volume increases of the dentate gyrus were larger in remitted patients than nonremitted patients; 2) ECT increased volumes in widely distributed brain regions, but not all changes were associated with clinical outcomes; 3) the largest volume increases in the right hippocampus and amygdala were associated with the number of ECT sessions and total seizure duration; and 4) ECT increased functional connectivity between the right hippocampus and ventromedial prefrontal cortex, which was associated with clinical improvement. These findings suggest that the antidepressant effect of ECT may be induced by a transient increase in hippocampal neuroplasticity and subsequent change in neuronal network. Research on the mechanism of ECT action has shifted to large-scale, multicenter research collaborations; however, in addition to the large-scale studies, basic research that can be compared with the results of clinical studies should be conducted. Another line of our research has focused on the stigma surrounding ECT. Patients who are referred for ECT sometimes cannot give consent because of their severe psychiatric symptoms, but such patients are considered as good candidates for ECT. Our survey found that over 80% of ECT patients were satisfied with ECT regardless of their consent status. Clinicians should be familiar with the ethical framework of nonvoluntary treatment and with clinical characteristics predictive for better ECT outcomes when they provide ECT without patients' consent but with their relatives' consent. Thorough discussion with international researchers and ethics experts about nonvoluntary ECT is needed for appropriate ECT provision.
 Author's abstract