Abstract:Objective To investigate the changes of resting-state functional connectivity and brain network metrics in the response inhibition-related cortices after anodal high definition transcranial direct current stimulation (HD-tDCS) on the right inferior frontal gyrus (rIFG) by resting-state functional near-infrared spectroscopy (fNIRS) imaging. Methods The experiment followed a 2 (stimulation type: rIFG stimulation vs sham stimulation)×2 (detecting time: pre-stimulation vs post-stimulation) 2-factor mixed design. A group of 48 healthy college students were enrolled and randomly divided into rIFG stimulation and sham stimulation groups (n=24). Resting-state fNIRS was used to record the changes of oxyhemoglobin, deoxyhemoglobin (HbR) and total hemoglobin (HbT) signals for 7 min before and after a single anodic HD-tDCS (1.25 mA, 20 min) stimulation of rIFG. The functional connectivity from region of interest to region of interest (ROI2ROI), functional connectivity matrices, and brain network efficiency indicators were analyzed for the key cortices of response inhibition (rIFG and right pre-supplementary motor area [pre-SMA]). Results The ROI2ROI functional connectivity analysis based on HbR signals showed that compared with the sham stimulation group, the functional connectivity between rIFG and right pre-SMA was significantly elevated in the rIFG stimulation group (P<0.05); the results of the functional connectivity matrix analysis revealed that the functional connectivity between channel 2 and channel 24 was significantly improved in the rIFG stimulation group than that in the sham stimulation group (P<0.001). The graph theory analysis based on HbT signals showed that the nodal efficiency delta values of channels 1, 5, 8, 9, 12, 19 and 26 in the rIFG stimulation group were significantly higher than those in the sham stimulation group (all corrected P<0.05). Conclusion Anodal HD-tDCS on the rIFG significantly enhances the functional connectivity between rIFG and right pre-SMA and increases the nodal efficiency of the response inhibition cortical network.