The contributions of the basal ganglia to motor control are apparent from the deficits that result from damage to the component nuclei. Such lesions compromise the initiation and performance of voluntary movements, as exemplified by the paucity of movement typical of Parkinson’s disease and in the inappropriate “release” of movements characteristic of Huntington’s disease. The organization of the basic circuitry of the basal ganglia indicates how this constellation of nuclei modulates movement. With respect to motor function, the system forms a loop that originates in almost every area of the cerebral cortex and eventually terminates, after enormous convergence within the basal ganglia, on the upper motor neurons in the motor and premotor areas of the frontal lobe and in the superior colliculus. The efferent neurons of the basal ganglia influence the upper motor neurons in the cortex by gating the flow of information through relays in the ventral nuclei of the thalamus. The upper motor neurons in the superior colliculus that initiate saccadic eye movements are controlled by monosynaptic projections from the substantia nigra pars reticulata. In each case, the basal ganglia loops regulate movement by a process of disinhibition that results from the serial interaction within the basal ganglia circuitry of two sets of GABAergic neurons. Internal circuits within the basal ganglia system modulate the amplification of the signals that are transmitted through the loops.