2006; Shemmell

et al 2009) The existence of separable s

2006; Shemmell

et al. 2009). The existence of separable spinal-and cortical-level Nutlin-3a manufacturer inhibitory effects within the TMS-induced silent period is informed by evidence that H-reflexes elicited within the silent period recover to baseline levels before the end of the silent period (Fuhr et al. 1991) and that stimulation of descending motor pathways at the level of the Inhibitors,research,lifescience,medical cervicomedullary junction induces a silent period of ~50 msec, significantly shorter than that induced by TMS (Inghilleri et al. 1993). The application of TMS results in an auditory “click” that may have influenced the subjects’ reaction time when instructed to resist an imposed perturbation. We controlled for this possibility by masking the Inhibitors,research,lifescience,medical sound of the TMS click with recordings of the same sound played at random intervals during each trial. We also included a sham stimulation condition in which the TMS coil was positioned on the scalp perpendicular to its most effective orientation (Fig. 1A). Although a magnetic field is still produced at the scalp in this orientation, its strength is far smaller

than at the center of the coil and sham TMS applied in this manner failed to induce any excitatory or suppressive responses in Inhibitors,research,lifescience,medical the ongoing EMG trace from the ECR (Fig. 1B). This was true for all participants. Subjects were not aware of whether TMS would be applied in any given trial. Data processing and analysis EMG recordings were rectified and averaged across all 20 trials in each experimental condition Inhibitors,research,lifescience,medical before further processing. All EMGs are expressed in mV of electrical activity recorded at the skin. Background EMG was quantified as the mean of the EMG within the period of 50–70 msec before perturbation onset, the period immediately before the application of TMS. The onset latencies of the short-and long-latency responses were determined visually within appropriate

time windows (SLSR: 10–40 msec after perturbation Inhibitors,research,lifescience,medical onset, LLSR: 40–80 msec after perturbation onset). The onset latency of each response was determined from data obtained in sham TMS conditions and the same onset latencies assumed for trials with TMS. For each perturbation, long-latency response amplitudes were quantified as the mean of the tuclazepam rectified EMG signal over a 20 msec time window after response onset. For sham TMS trials, reflex amplitudes were quantified relative to the background EMG before perturbation onset. For TMS trials, reflexes were quantified relative to the mean EMG measured during the silent period of the TMS-only trials, corresponding to the time period used for reflex calculations. Levels of background activity were matched in each experiment, and trials were eliminated off-line if the background muscle activity exceeded the mean of 20 trials ± 1.5 SD (~5% of trials).

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