The Putamen is a large subcortical nucleus that forms the lateral portion of the striatum, the major input structure of the basal ganglia. As a critical component of the motor loop, the putamen is essential for movement initiation, execution, habit formation, and reward processing. This page provides comprehensive information about its anatomical structure, physiological functions, neurochemical properties, and pivotal role in neurodegenerative diseases, particularly Parkinson's disease (PD) and Huntington's disease (HD). [1]
| Property | Value | [2]
|----------|-------| [3]
| Category | Dorsal Striatum, Basal Ganglia | [4]
| Location | Lateral portion of the striatum, dorsal to the globus pallidus, lateral to the caudate nucleus | [5]
| Cell Types | Medium spiny neurons (D1 and D2), fast-spiking interneurons, low-threshold spiking interneurons, cholinergic interneurons | [6]
| Primary Neurotransmitters | GABA (output), Dopamine (modulation) | [7]
| Key Markers | DARPP32, D1R, D2R, PV (parvalbumin), Calbindin, Enkephalin |
| Volume (human) | Approximately 5-6 cm³ total |
| Cell Count | ~100 million neurons in adult human |
The putamen is located in the basal ganglia, deep within the cerebral hemispheres:
The putamen contains diverse neuronal populations:
The putamen exhibits neurochemical compartmentalization:
The putamen is a central hub for motor control:
Motor Cortex → Putamen (D1-MSNs) → GPi/SNr → Thalamus → Motor Cortex (Facilitated)
Motor Cortex → Putamen (D2-MSNs) → GPe → STN → GPi/SNr → Thalamus → Motor Cortex (Inhibited)
The putamen processes reward-related information:
Beyond motor control, the putamen contributes to:
Dopamine from the substantia nigra pars compacta (SNc) critically modulates putamen function:
| Receptor Type | Pathway | Effect of Dopamine | Effect in PD |
|---|---|---|---|
| D1 (D1-MSNs) | Direct | Excitatory | ↓ Movement initiation |
| D2 (D2-MSNs) | Indirect | Inhibitory (disinhibition) | ↑ Movement inhibition |
MSNs produce GABA as their primary neurotransmitter:
Cholinergic interneurons (TANs) play important roles:
The putamen is severely affected in PD:
The putamen shows early and severe degeneration in HD:
| Disease | Putamen Involvement | Clinical Relevance |
|---|---|---|
| Multiple System Atrophy (MSA) | Striatal degeneration | Severe motor impairment |
| Progressive Supranuclear Palsy | Tau pathology in striatum | Falls, parkinsonism |
| Corticobasal Degeneration | Asymmetric putaminal atrophy | Apraxia, rigidity |
| Dementia with Lewy Bodies | Lewy body pathology | Cognitive fluctuations |
| Source | Neurotransmitter | Function |
|---|---|---|
| Motor Cortex | Glutamate | Movement initiation |
| Premotor Cortex | Glutamate | Movement planning |
| Supplementary Motor Area | Glutamate | Sequence planning |
| Somatosensory Cortex | Glutamate | Sensory feedback |
| Thalamus (centromedian/parafascicular) | Glutamate | Modulatory input |
| Substantia Nigra pars compacta | Dopamine | Reward/motor modulation |
| Raphe Nuclei | Serotonin | Mood/motivation modulation |
| Target | Pathway | Effect |
|---|---|---|
| Globus Pallidus externus (GPe) | D2-MSNs (indirect) | Inhibition → movement suppression |
| Globus Pallidus internus (GPi) | D1-MSNs (direct) | Inhibition → movement facilitation |
| Substantia Nigra pars reticulata (SNr) | D1-MSNs (direct) | Inhibition → movement facilitation |
The study of Putamen has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development.
Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.
Graybiel AM. Habits, rituals, and the evaluative brain. Annu Rev Neurosci. 2008;31:359-387. 2008. ↩︎
Obeso JA, Rodriguez-Oroz MC, Benitez-Temino B, et al. Functional organization of the basal ganglia: therapeutic implications for Parkinson's disease. Mov Disord. 2008;23(Suppl 3):S548-S559. 2008. ↩︎
[Albin RL, Young AB, Penney JB. The functional anatomy of basal ganglia disorders. Trends Neurosci. 1989;12(10):366-375](https://doi.org/10.1016/0166-2236(89). 1989. ↩︎
DeLong MR, Wichmann T. Circuits and circuit disorders of the basal ganglia. Arch Neurol. 2007;64(1):20-24. 2007. ↩︎
[Parent A, Hazrati LN. Functional anatomy of the basal ganglia. I. The cortico-striato-pallido-thalamo-cortical loop. Brain Res Rev. 1995;20(1):91-127](https://doi.org/10.1016/0165-0173(94). 1995. ↩︎
Kreitzer AC, Malenka RC. Striatal plasticity and basal ganglia circuit function. Nature. 2008;455(7213):643-649. 2008. ↩︎
[Surmeier DJ, Song WJ, Yan Z. The origins of the dopaminergic innervation of the dorsal striatum. J Comp Neurol. 1996;364(3):540-554](https://doi.org/10.1002/(SICI). 1996. ↩︎