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In humans, finely tuned gamma synchronization (60-90 Hz) rapidly appears at movement onset in a motor control network involving primary motor cortex, the basals ganglia and motor thalamus. Yet the functional consequences of brief movement-related synchronization are still unclear. Distinct synchronization phenomena have also been linked to different forms of motor inhibition, including relaxing antagonist muscles, rapid movement interruption and stabilizing network dynamics for sustained contractions. Here I will introduce detailed hypotheses about how intra- and inter-site synchronization could interact with firing rate changes in different parts of the network to enable flexible action control. The here proposed cause-and-effect relationships shine a spotlight on potential key mechanisms of cortico-basal ganglia-thalamo-cortical communication. Confirming or revising these hypotheses will be critical in understanding the neuronal basis of flexible movement initiation, invigoration and inhibition. Ultimately, the study of more complex cognitive phenomena will also become more tractable once we understand the neuronal mechanisms underlying behavioural readouts.Significance statementIn spite of tremendous progress in describing how neuronal activity unfolds before and during movements, the mechanisms that trigger the switch from movement preparation to execution, regulate movement vigour and enable movement inhibition remain unknown. Brief synchronization of neural activity within and between cortical sites and the basal ganglia may be a key factor in controlling these mechanisms. Here I review the evidence and describe in detail how synchronization may shape firing rates in distinct sites of the cortico-basal ganglia-thalamo-cortical network to enable flexible action control.

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Beta, Gamma, STN, inhibition, movement vigour, phase coupling