2002; MacKinnon et al. 2007) and as participants were asked to counteract a bias force toward wrist flexion, we know that a command for wrist extension (ECR contraction) existed prior to

each stimulus. Also, in support of this idea is evidence that TMS is capable of eliciting short-latency responses in neurons of the reticular formation in monkeys (Fisher et al. 2012). It is not clear, however, whether the activation of startle reflex circuits is responsible for the difference in LLSR amplitude between TMS of the contralateral and ipsilateral hemispheres. While there is some evidence that muscular responses to startle circuit activation Inhibitors,research,lifescience,medical are lateralized (selleck screening library Grillon and Davis 1995), the preferential activation of muscles ipsilateral to the auditory stimulus is yet to be demonstrated. Taken together, our results and those of previous studies suggest that the primary motor cortex ipsilateral to a perturbed wrist is not involved in generation

or modulation Inhibitors,research,lifescience,medical of the LLSR, although there is some suggestion that it could play a role in regulating the reflex through transcallosal inhibitory effects. Neither primary motor cortex regulates the gain of the LLSRs in wrist extensor muscles Inhibitors,research,lifescience,medical While TMS-induced suppression of the right motor cortex reduced the amplitude of the LLSR, it did not reduce the stability-dependent modulation of the reflex between stiff and compliant conditions. Our hypothesis Inhibitors,research,lifescience,medical that this suppression would reduce stability-dependent modulation of the LLSR was based on previous findings demonstrating that LLSR modulation in more proximal muscles is reduced during similar TMS-induced suppression of activity in the primary motor cortex (Kimura et al. 2006; Shemmell et al. 2009). During Inhibitors,research,lifescience,medical movement, motor cortex suppression appears to eliminate modulation of the LLSR that is due to anticipated arm perturbations (Kimura et al. 2006). During postural maintenance, the same motor

cortex suppression reduces LLSR modulation that occurs due to changes in environmental stability, but does not eliminate it entirely (Shemmell et al. 2009). Our current results demonstrate PD184352 (CI-1040) that stability-related LLSR modulation in a more distal muscle, the ECR, is not reduced by motor cortex suppression. When considered in the context of previous findings, our results support the idea that when the goal of a task is to maintain a consistent posture, the primary motor cortex is involved in the transmission of a transcortical stretch reflex but is not the primary locus of reflex gain regulation. The nature of motor cortex involvement may change during movement, where it appears to assume more responsibility for regulating rapid corrective actions (Fromm and Evarts 1977; Maier et al. 1993), although this is not likely achieved through reflex regulation as stretch reflexes are inhibited during the corrective phase of rapid movements (Gottlieb et al. 1983).