091 ± 0.098 mV, TMS: 0.073 ± 0.010 mV; P = 0.036) environments (Fig. 3A and B). Figure 3 (A) The average amplitude of recorded EMG is shown during time periods representing tonic muscle activation prior to any stimuli (background [BGD]) and the LLSR. Responses following stimulation of the contralateral (right) motor cortex are designated Inhibitors,research,lifescience,medical … Hypothesis 3: that inhibiting the ipsilateral (left) primary motor cortex would reduce the amplitude of the LLSR. Contrary to
our hypothesis, applying supramotor threshold TMS to the primary motor cortex ipsilateral to the target ECR did not reduce the amplitude of the LLSR in either mechanical environment (Fig. 2B and D). The amplitude of LLSRs induced within the period of ipsilateral motor cortex inhibition was not different to that of LLSRs induced during sham stimulation in either stiff (sham: 0.087 ± 0.091 mV, TMS: 0.108 ± 0.128 mV; P = 0.152) or compliant Inhibitors,research,lifescience,medical (sham: 0.111 ± 0.092 mV, TMS: 0.122 ± 0.114 mV; P = 0.27) environments. Interestingly, Inhibitors,research,lifescience,medical LLSR amplitude was greater when sham TMS was applied to the ipsilateral (stiff: 0.087 ± 0.091 mV, compliant: 0.111 ± 0.092 mV), compared to the contralateral (stiff: 0.059 ± 0.062 mV [P = 0.044], compliant: 0.091 ± 0.098 mV
[P = 0.043]) motor cortex. Hypothesis 4: that inhibiting the contralateral primary motor cortex would reduce modulation of the LLSR between stiff and compliant mechanical environments. Contrary to our predictions and to evidence of the involvement of the contralateral motor cortex in LLSR gain modulation (Shemmell et al. 2009, 2010), inhibition of the contralateral hemisphere Inhibitors,research,lifescience,medical failed to reduce the change
in LLSR amplitude between stiff and compliant environments (change in LLSR during sham: 0.032 ± 0.042 mV, Inhibitors,research,lifescience,medical change in LLSR during TMS: 0.030 ± 0.051 mV; P = 0.847; Fig. 3A and B). Hypothesis 5: that inhibiting the ipsilateral primary motor cortex would reduce modulation of the LLSR between stiff and compliant mechanical environments. Compared to sham, TMS-induced inhibition of the ipsilateral most motor cortex did not significantly alter the extent of amplitude modulation of the LLSR between the stiff and compliant environments (change in LLSR during sham: 0.024 ± 0.033 mV, change in LLSR during TMS: 0.013 ± 0.042 mV; P = 0.164; Fig. 3A and B). Discussion The results of this study check details demonstrate that, in normal participants, the contralateral but not ipsilateral motor pathway is involved in stability-dependent modulation of the LLSR in a wrist extensor muscle. The results extend previous findings suggesting that the contralateral primary motor cortex is involved in the transmission of the LLSR, although they suggest that the locus of gain regulation for this reflex response resides outside the motor cortex.