Changes in the cortical silent period during force control.

These findings indicate that the excitability of gamma-aminobutyric acidergic inhibitory neural circuits in primary motor cortex decreases in response to increased force output, mediated via increased corticospinal and motoneuron excitability. These results may facilitate understanding of the role of the gamma-aminobutyric acidergic circuit in primary motor cortex in force control, as well as of the mechanism underlying motor dysfunction in stroke-induced palsy, dystonia, and cerebellar ataxia.