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This study aimed to determine how transcutaneous vagus nerve stimulation (tVNS) alters autonomic nervous activity by comparing the effects of different tVNS frequencies and current intensities. We also investigated the sex-dependent autonomic response to tVNS. Thirty-five healthy adult participants were stimulated using a tVNS stimulator at the left cymba conchae while sitting on a reclining chair; tVNS-induced waveform changes were then recorded for different stimulus frequencies (Experiment 1: 3.0 mA at 100 Hz, 25 Hz, 10 Hz, 1 Hz, and 0 Hz (no stimulation)) and current intensities (Experiment 2: 100 Hz at 3.0 mA, 1.0 mA, 0.2 mA (below sensory threshold), and 0 mA (no stimulation)) using an electrocardiogram. Pulse widths were set at 250 µs in both experiment 1 and 2. Changes in heart rate (HR), root-mean-square of the difference between two successive R waves (RMSSD), and the ratio between low-frequency (LF) (0.04–0.15 Hz) and high-frequency (HF) (0.15–0.40 Hz) bands (LF/HF) in spectral analysis, which indicates sympathetic and parasympathetic activity, respectively, in heart rate variability (HRV), were recorded for analysis. Although stimulation at all frequencies significantly reduced HR (p = 0.001), stimulation at 100 Hz had the most pronounced effect (p = 0.001) in Experiment 1 and was revealed to be required to deliver at 3.0 mA in Experiment 2 (p = 0.003). Additionally, participants with higher baseline sympathetic activity experienced higher parasympathetic response during stimulation, and sex differences may exist in the autonomic responses by the application of tVNS. Therefore, our findings suggest that optimal autonomic changes induced by tVNS to the left cymba conchae vary depending on stimulating parameters and sex.

Motor evoked potentials (MEPs) evoked by transcranial magnetic stimulation (TMS) a few milliseconds after this cortical activity following electrical stimulation (ES) result in an inhibition comparable to that by TMS alone; this is called short-latency afferent inhibition (SAI). Cortical activity is observed after mechanical tactile stimulation (MS) and is affected by the number of stimuli by ES. We determined the effects of somatosensory stimulus methods and multiple conditioning stimuli on SAI in 19 participants. In experiment 1, the interstimulus intervals between the conditioning stimulation and TMS were 25, 27 and 29 ms for ES and 28, 30 and 32 ms for MS. In experiment 2, we used 1, 2, 3 and 4 conditioning stimulations of ES and MS. The interstimulus interval between the ES or MS and TMS was 27 or 30 ms, respectively. In experiment 1, MEPs were significantly decreased in both the ES and MS conditions. In experiment 2, MEPs after ES were significantly decreased in all conditions. Conversely, MEPs after MS were significantly decreased after one stimulus and increased after four stimulations, indicating the SAI according to the number of stimuli. Therefore, the somatosensory stimulus methods and multiple conditioning stimuli affected the SAI.

The Met allele of the brain-derived neurotrophic factor (BDNF) gene confers reduced cortical BDNF expression and associated neurobehavioral changes. BDNF signaling influences the survival, development, and synaptic function of cortical networks. Here, we compared gamma-aminobutyric acid (GABA)ergic network activity in the human primary motor cortex (M1) between the Met (Val/Met and Met/Met) and non-Met (Val/Val) genotype groups. Short- and long-interval intracortical inhibition, short-latency afferent inhibition (SAI), and long-latency afferent inhibition were measured using transcranial magnetic stimulation (TMS) as indices of GABAergic activity. Furthermore, the considerable inter-individual variability in inhibitory network activity typically measured by TMS may be affected not only by GABA but also by other pathways, including glutamatergic and cholinergic activities; therefore, we used 3-T magnetic resonance spectroscopy (MRS) to measure the dynamics of glutamate plus glutamine (Glx) and choline concentrations in the left M1, left somatosensory cortex, and right cerebellum. All inhibitory TMS conditions produced significantly smaller motor-evoked potentials than single-pulses. SAI was significantly stronger in the Met group than in the Val/Val group. Only the M1 Glx concentration was significantly lower in the Met group, while the BDNF genotype did not affect choline concentration in any region. Further, a positive correlation was observed between SAI and Glx concentrations only in M1. Our findings provide evidence that the BDNF genotype regulates both the inhibitory and excitatory circuits in human M1. In addition, lower Glx concentration in the M1 of Met carriers may alter specific inhibitory network on M1, thereby influencing the cortical signal processing required for neurobehavioral functions.

The supplementary motor area (SMA) may modulate spinal reciprocal inhibition (RI) because the descending input from the SMA is coupled to interneurons in the spinal cord via the reticulospinal tract. Our study aimed to verify whether the anodal transcranial direct current stimulation (anodal-tDCS) of the SMA enhances RI. Two tDCS conditions were used: the anodal stimulation (anodal-tDCS) and sham stimulation (sham-tDCS) conditions. To measure RI, there were two conditions: one with the test stimulus (alone) and the other with the conditioning-test stimulation intervals (CTIs), including 2 ms and 20 ms. RI was calculated at multiple time points: before the tDCS intervention (Pre); at 5 (Int 5) and 10 min; and immediately after (Post 0); and at 5, 10 (Post 10), 15, and 20 min after the intervention. In anodal-tDCS, the amplitude values of H-reflex were significantly reduced for a CTI of 2 ms at Int 5 to Post 0, and a CTI of 20 ms at Int 5 to Pot 10 compared with Pre. Stimulation of the SMA with anodal-tDCS for 15 min activated inhibitory interneurons in RIs by descending input from the reticulospinal tract via cortico–reticulospinal projections. The results showed that 15 min of anodal-tDCS in the SMA enhanced and sustained RI in healthy individuals.