Abstract

Changes in neural activity occur in the motor cortex prior to movement, but the nature and purpose of this preparatory activity is unclear. To investigate this in the human (male and female) brain non-invasively, we used transcranial magnetic stimulation (TMS) to probe the excitability of distinct sets of excitatory inputs to corticospinal neurones during the warning period of various reaction time tasks. Using two separate methods (H-reflex conditioning and directional effects of TMS), we show that a specific set of excitatory inputs to corticospinal neurones are suppressed during motor preparation, whilst another set of inputs remain unaffected. To probe the behavioural relevance of this suppression, we examined whether the strength of the selective preparatory inhibition in each trial was related to reaction time. Surprisingly, the greater the amount of selective preparatory inhibition, the faster the reaction time was. This suggests that the inhibition of inputs to corticospinal neurones is not involved in preventing release of movement but may in fact facilitate rapid reactions. Thus, selective suppression of a specific set of motor cortical neurones may be a key aspect of successful movement preparation.

Significance statement

Movement preparation evokes substantial activity in the motor cortex despite no apparent movement. One explanation for the lack of movement is that motor cortical output in this period is gated by an inhibitory mechanism. This notion was supported by previous non-invasive TMS studies of human motor cortex indicating a reduction of corticospinal excitability. On the contrary, our data supports the idea that there is a coordinated balance of activity upstream of the corticospinal output neurones. This includes a suppression of specific local circuits that supports, rather than inhibits, the rapid generation of prepared movements. Thus, the selective suppression of local circuits appears to be an essential part of successful movement preparation, instead of an external control mechanism.