Your brain moves by releasing a brake, not by pressing an accelerator
Deep in the forebrain, the basal ganglia keep the body's motor systems under constant restraint. Their output neurons fire steadily at high rates, suppressing movement, and an action happens only when that suppression briefly lifts. When the circuit falters, the results range from the tremor of Parkinson's disease to the tics of Tourette syndrome.
The basal ganglia are clusters of grey matter buried near the thalamus, mirrored on left and right. Anatomists divide them into four parts: two large ones, the striatum and the pallidum, and two smaller ones, the substantia nigra and the subthalamic nucleus. The striatum, the biggest, collects signals from much of the brain but sends its output only to other parts of the basal ganglia. Beyond movement, the group is linked with habit formation, procedural learning, eye movements, emotion and cognition.
Most of the circuitry is inhibitory. Pallidal neurons, which use the transmitter GABA, fire continuously when left alone, and input from the striatum makes them pause. Because they normally hold the thalamus in check, a pause releases it, a principle called disinhibition. The subthalamic nucleus is the only component that sends excitatory signals, using glutamate to drive the inhibitory output further. The pars compacta of the substantia nigra supplies dopamine, which keeps the striatal pathways balanced.
A widely used model from the 1990s, proposed by DeLong, splits the flow into a direct pathway that frees the thalamus and an indirect one that restrains it. Timing problems with that scheme led researchers to add a fast hyperdirect route running from the cortex through the subthalamic nucleus, and the neat division between pathways is now questioned. Circuits are also described as parallel loops, commonly grouped into motor, associative and limbic domains, and the system is thought to help select not only which movement to make but perhaps which thought to pursue.
Damage shows how much depends on it. Parkinson's disease involves the loss of dopamine-producing cells in the substantia nigra, Huntington's disease mainly damages the striatum, and obsessive-compulsive disorder and addiction are also tied to basal ganglia dysfunction. A limbic sector that includes the nucleus accumbens appears central to reward.
Source: Basal ganglia
