The striatum is a large cluster of neurons deep in the brain, and it’s built from two main divisions: the dorsal striatum (made up of the caudate nucleus and the putamen) and the ventral striatum (centered on the nucleus accumbens). These structures work together as the primary input hub of the basal ganglia, receiving signals from across the brain and routing them into circuits that control movement, decision-making, and motivation.
Dorsal and Ventral Divisions
The dorsal striatum, consisting of the caudate nucleus and the putamen, handles most of the brain’s sensory and motor processing. These two structures receive the bulk of their input from cortical areas involved in movement and sensation. The caudate curves along the wall of the brain’s fluid-filled ventricles and plays a larger role in goal-directed planning, while the putamen sits closer to the outer edge of the brain and is more directly involved in executing learned movements.
The ventral striatum sits below and slightly in front of its dorsal counterpart. Its centerpiece is the nucleus accumbens, which is further split into two zones: the shell and the core. The core is linked to subjective decision-making, helping weigh factors like effort, risk, and delay when choosing between options. The shell tracks the actual outcome value of rewards. In rat studies, dopamine release in the shell was significantly higher and longer lasting than in the core when animals responded to cues signaling different reward sizes, and shell dopamine also spiked during reward consumption itself. The ventral striatum receives most of its input not from motor areas but from brain regions that process emotion and memory, including the amygdala, hippocampus, and prefrontal cortex.
The Cells Inside the Striatum
About 95% of all striatal neurons are a single cell type: medium spiny neurons (sometimes called spiny projection neurons). These are the workhorses of the striatum. They use the inhibitory neurotransmitter GABA, meaning they quiet the activity of whatever they connect to rather than exciting it. Medium spiny neurons come in two distinct populations that are intermingled throughout the striatum but differ in what receptors they carry and where they send their signals.
The remaining roughly 5% are interneurons, cells that don’t project out of the striatum but instead shape local activity. Four main types have been identified based on their size and the chemical markers they express:
- Cholinergic interneurons: the largest cells in the striatum, with nuclei around 12 micrometers across. They release acetylcholine and act as modulators of striatal circuits.
- Parvalbumin-expressing interneurons: fast-firing cells with elongated nuclei, capable of powerfully inhibiting nearby medium spiny neurons.
- Somatostatin-expressing interneurons: smaller cells with distinctly elongated, spindle-shaped bodies.
- Calretinin-expressing interneurons: the smallest of the group, with compact nuclei.
Two Opposing Pathways
The two populations of medium spiny neurons form the basis of the striatum’s most important organizational principle: the direct and indirect pathways. These pathways have opposite effects on movement and behavior, and the split comes down to which dopamine receptor each neuron carries. The separation is remarkably clean. D1 and D2 receptors are segregated in all but fewer than 2% of striatal neurons.
Neurons in the direct pathway carry D1 dopamine receptors. When activated, they inhibit a downstream relay station, which itself normally inhibits the thalamus. The result is a double negative: the thalamus is released from inhibition and can drive the cortex to produce movement. This is why the direct pathway is described as promoting action.
Neurons in the indirect pathway carry D2 dopamine receptors. They add a third inhibitory link to the chain, and the net result flips: thalamic activity gets suppressed, and movement is held back. Dopamine stimulates D1 neurons and inhibits D2 neurons, so when dopamine is present in the striatum, the balance tips toward action. When dopamine drops, as it does in Parkinson’s disease, the indirect pathway dominates and movement becomes difficult.
Striosomes and Matrix
Beyond the division into dorsal and ventral, the striatum has a second, finer-grained organizational layer. When stained for certain chemical markers, the tissue doesn’t look uniform. Instead, it reveals a mosaic of two interlocking compartments: striosomes (also called patches) and the surrounding matrix. These compartments differ in their chemical makeup, the brain regions they connect to, and how their synapses are regulated. Three decades of study have established that striosomes and matrix are not just cosmetically different under a microscope. They receive partially distinct inputs and send their outputs to partially different targets, and recent work suggests the synapses within each compartment are regulated by different neurochemical interactions.
Inputs That Drive the Striatum
The striatum doesn’t generate its own activity. It depends on excitatory input from two major sources: the cerebral cortex and the thalamus. Both deliver their signals using the neurotransmitter glutamate, which excites medium spiny neurons and triggers the cascading inhibitory output that the striatum is known for. Motor cortex in particular sends massive projections to the striatum, providing the information needed to shape motor behavior. Thalamic inputs target sensorimotor regions and help the striatum process functionally distinct streams of information in parallel.
The other critical input is dopamine, arriving from neurons in the midbrain. Dopamine doesn’t simply excite or inhibit the striatum. It modulates how striatal neurons respond to their cortical and thalamic inputs, effectively setting the gain on the entire system. This is why dopamine-related disorders produce such dramatic effects on movement and motivation.
Blood Supply
The striatum sits deep in the brain, far from the surface arteries, so it relies on small penetrating vessels called striate arteries. The most important of these are the lenticulostriate arteries, which branch off the middle cerebral artery as it travels along the base of the frontal lobe. A second set of branches, including the recurrent artery of Heubner (also called the distal medial striate artery), arises from the anterior cerebral artery. Both groups ascend through a region at the base of the brain called the anterior perforated substance before reaching the deep structures of the basal ganglia. Because these are small end-arteries with limited backup supply, blockages here are a common cause of a particular type of stroke affecting deep brain tissue.
What Happens When the Striatum Breaks Down
The striatum’s heavy reliance on a single dominant cell type makes it especially vulnerable to disease. In Huntington’s disease, a genetic mutation causes severe, progressive degeneration of the striatum, with medium spiny neurons bearing the worst losses. The caudate and putamen visibly shrink on brain scans as the disease progresses, and the loss of these output neurons disrupts both the direct and indirect pathways, producing the involuntary movements and cognitive decline characteristic of the condition.
In Parkinson’s disease, the striatum itself doesn’t degenerate, but it loses the dopamine input it depends on. As midbrain dopamine neurons die, the balance between the direct and indirect pathways shifts. Without dopamine to stimulate D1 neurons and quiet D2 neurons, the indirect pathway becomes overactive, the thalamus is excessively inhibited, and initiating movement becomes increasingly difficult. The tremor, stiffness, and slowness of Parkinson’s disease are all downstream consequences of a striatum starved of dopamine.