We sought to understand the basic neural processes involved in the functional linking of motor cortical points. We asked which of the two basic neural mechanisms, excitation or inhibition, is required to functionally link motor cortical points. In the ketamine-anaesthetized cat, a microstimulation electrode was positioned at a point (control point) that was identified by the following three characteristics of the EMG responses: the muscle(s) activated at threshold, any additional muscles recruited by supra-threshold stimulation, and their relative latency. A second distinct point (test point) producing activation of a muscle at a different joint was then identified. At this test cortical point the GABA(A) receptor antagonist bicuculline was ejected iontophoretically, while stimulating the control point near threshold. A combined response was elicited consisting of the response normally elicited at the control point plus that elicited at the test point. Thus, an artificial muscle synergy was produced following disinhibition of the test point. This was never the case when glutamate was ejected at the test point, even when supra-threshold stimuli were used at the control point. Therefore, simply increasing the excitability of a cortical point was not sufficient to release the muscle(s) represented at that point into a muscle synergy. Kynurenate, a broadly acting excitatory amino acid receptor antagonist, ejected at the bicuculline point reversed the effect of bicuculline. This shows that the release phenomenon was mediated synaptically and was not due to spread of the stimulating current. We suggest that release from inhibition may be one of the neural mechanisms involved in functionally linking motor cortical points. This functional linking may be part of the ensemble of motor cortical mechanisms involved in recruitment of muscle synergies.