6 RMT (Kujirai et al., 1993). As observed previously (Ziemann et al., 1996), no ICF could be evoked with such low conditioning stimuli, and increasing its intensity to the threshold for ICF (0.8 RMT) was not possible because the conditioning pulse by itself could evoke a peak in the PSTH (see below, Protocol 1). Based on our previous study (Lackmy MK-1775 mouse & Marchand-Pauvert, 2010), Protocol 1 was first elaborated to test the influence

of the test peak on SICI. Experiments were performed on 27 motor units from ten subjects. The test pulse intensity was changed in a range defined by the threshold intensity for evoking a significant peak in the PSTH (0.75 ± 0.02 RMT), and an intensity

corresponding to RMT minus 5% the maximal stimulator output (MSO; Fisher et al., 2002); for example, RMT was 51% MSO in the subject illustrated in Fig. 2, and the maximal test intensity was 46%, i.e. about 0.90 RMT. Only test intensities below the motor selleckchem threshold were investigated, because if an MEP occurred in the EMG activity, it could interfere with the recording of the motor unit discharge due to superimposition of MEP and motor unit potential. The test intensity was randomly changed from one recording to another and, at the end of the experiment, we ensured that each TMS intensity (in 1% steps), between peak threshold and RMT minus 5% MSO, had been tested. The intensity of the test pulse was then normalized to RMT for inter-individual comparisons (Fig. 2A,D and G). About 10–12 recording sessions were made for each motor unit, one recording session for each intensity investigated. Each recording session lasted 4–7 min. The hot spot for FDI was determined at the beginning of the experiment, and marked on the scalp in Protocol 1. Although the conditioning pulse intensity was kept constant throughout the experiment (0.6 RMT), a minimal change of the coil orientation might have influenced the stimulating conditions, and therefore the level of SICI: something that can be controlled only by monitoring stimulus

intensity and stimulation site because the conditioning pulse (0.6 RMT) did not produce any significant change in the PSTH (Fig. 1C). This would also have influenced the effect of the Tobramycin test pulse, and thus the test peak size. To stabilize the stimulating conditions, a second protocol was developed with the NBS system to monitor the coil position and the TMS-induced electrical field in the brain. Based on the results of Protocol 1, we adjusted the TMS test intensity to 0.75 and 0.85 RMT to evoke small and medium peaks in the PSTH (∼10 and 20–30% the number of stimuli, respectively), and we increased TMS intensity to 0.95 RMT to explore SICI on larger test peaks than in Protocol 1 (> 30% the number of stimuli).