IntroductionUnlike the effect of repetitive transcranial magnetic stimulation (rTMS) in treating neuropsychiatric diseases, little is known about how personal factors might account for the disparity of results from studies of cognition and rTMS. In this study, we investigated the effects of high-frequency rTMS on response inhibition control and explored the time course changes in cognitive processing and brain metabolic mechanisms after rTMS using event-related potentials (ERPs) and magnetic resonance spectroscopy (1H-MRS).MethodsParticipants were all right-handed and were naive to rTMS and the Go/NoGo task. Twenty-five healthy young participants underwent one 10 Hz rTMS session per day in which stimulation was applied over the left dorsolateral prefrontal cortex (DLPFC), and a homogeneous participant group of 25 individuals received a sham rTMS treatment for 1  week. A Go/NoGo task was performed, an electroencephalogram (EEG) was recorded, and1H-MRS was performed.ResultsThe results revealed that there was a strong trend of decreasing commission errors of NoGo stimuli by high frequency rTMS over the left DLPFC, whereas there was no significant difference between before and after rTMS treatment with respect to these parameters in the sham rTMS group. High-frequency rTMS significantly increased the amplitude of NoGo-N2 but not Go-N2, Go-P3, or NoGo-P3. The myo-inositol /creatine complex (MI/Cr) ratio, indexing cerebral metabolism, in the left DLPFC was decreased in the rTMS treated group.DiscussionThis observation supports the view that high-frequency rTMS over the left DLPFC has the strong tendency of reducing commission errors behaviorally, increase the amplitude of NoGo-N2 and improve the response inhibition control of healthy young participants. The results are consistent with the excitatory properties of high frequency rTMS. We suggest that the increase in the NoGo-N2 amplitude may be related to the increased excitability of the DLPFC-anterior cingulate cortex (ACC) neural loop. Metabolic changes in the DLPFC may be a possible mechanism for the improvement of the response inhibition control of rTMS.