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Striatum
Striatum shown in green with other basal ganglia and thalamus. Small region in yellow is the amygdala
Tractography showing corticostriatal connections
Details
Part ofBasal ganglia[1]
Reward system[2][3]
PartsVentral striatum[2][3][4]
Dorsal striatum[2][3][4]
Identifiers
Latinstriatum
MeSHD003342
NeuroNames225
NeuroLex IDbirnlex_1672
TA98A14.1.09.516
A14.1.09.515
TA25559
FMA77616 77618, 77616
Anatomical terms of neuroanatomy

The striatum (pl.: striata) or corpus striatum[5] is a cluster of interconnected nuclei that make up the largest structure of the subcortical basal ganglia.[6] The striatum is a critical component of the motor and reward systems; receives glutamatergic and dopaminergic inputs from different sources; and serves as the primary input to the rest of the basal ganglia.

Functionally, the striatum coordinates multiple aspects of cognition, including both motor and action planning, decision-making, motivation, reinforcement, and reward perception.[2][3][4] The striatum is made up of the caudate nucleus, the putamen, and the ventral striatum.[7] The lentiform nucleus is made up of the larger putamen, and the smaller globus pallidus.[8] Strictly speaking the globus pallidus is part of the striatum. It is common practice, however, to implicitly exclude the globus pallidus when referring to striatal structures.

In primates, the striatum is divided into the ventral striatum and the dorsal striatum, subdivisions that are based upon function and connections. The ventral striatum consists of the nucleus accumbens and the olfactory tubercle. The dorsal striatum consists of the caudate nucleus and the putamen. A white matter nerve tract (the internal capsule) in the dorsal striatum separates the caudate nucleus and the putamen.[4] Anatomically, the term striatum describes its striped (striated) appearance of grey-and-white matter.[9]

Structure

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The striatum as seen on MRI. The striatum includes the caudate nucleus and the lentiform nucleus which includes the putamen and the globus pallidus
The striatum in red as seen on MRI. The striatum includes the caudate nucleus (top), and the lentiform nucleus (the putamen (right) and the globus pallidus (lower left))

The striatum is the largest structure of the basal ganglia. The striatum is divided into two subdivisions, a ventral striatum and a dorsal striatum, based upon function and connections. It is also divisible into a matrix and embedded striosomes.

Ventral striatum

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The ventral striatum is composed of the nucleus accumbens and the olfactory tubercle.[4][10] The nucleus accumbens is made up of the nucleus accumbens core and the nucleus accumbens shell, which differ by neural populations. The olfactory tubercle receives input from the olfactory bulb but has not been shown to play a role in processing smell.[10] In non-primate species, the islands of Calleja are included.[11] The ventral striatum is associated with the limbic system and has been implicated as a vital part of the circuitry for decision making and reward-related behavior.[12][13]

Dorsal striatum

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The dorsal striatum is composed of the caudate nucleus and the putamen. Primarily it mediates cognition and involves motor and executive function. The dorsal striatum can be further subdivided into the dorsomedial striatum, and the dorsolateral striatum. Both of these areas have different roles in the acquisition of learnt behaviour and skill formation.[14] The dorsomedial region receives projections from the frontal and the parietal cortices. The dorsolateral region receives projections from the sensorimotor cortex.[15]

Matrix and striosomes

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Neurochemistry studies have used staining techniques on the striatum that have identified two distinct striatal compartments, the matrix, and the striosome (or patch). The matrix is seen to be rich in acetylcholinesterase, while the embedded striosomes are acetylcholinesterase-poor.[16] The matrix forms the bulk of the striatum, and receives input from most areas of the cerebral cortex.[17] Clusters of neurons in the matrix, called matrisomes receive a similar input. Their output goes to both regions of the globus pallidus and to the substantia nigra pars reticulata.[17]

The striosomes receive input from the prefrontal cortex and give outputs to the substantia nigra pars compacta.[17] There are more striosomes present in the dorsal striatum making up 10-15% of the striatal volume, than in the ventral striatum.[16]

Cell types

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Dendritic spines on medium spiny neuron of striatum

Types of cells in the striatum include:

  • Medium spiny neurons (MSNs), which are the principal neurons of the striatum.[2] They are GABAergic and, thus, are classified as inhibitory neurons. Medium spiny projection neurons comprise 95% of the total neuronal population of the human striatum.[2] Medium spiny neurons have two characteristic types: D1-type MSNs and D2-type MSNs.[2][4][18] A subpopulation of MSNs contain both D1-type and D2-type receptors, with approximately 40% of striatal MSNs expressing both DRD1 and DRD2 mRNA.[2][4][18]
  • Cholinergic interneurons release acetylcholine, which has a variety of important effects in the striatum. In humans, other primates, and rodents, these interneurons respond to salient environmental stimuli with stereotyped responses that are temporally aligned with the responses of dopaminergic neurons of the substantia nigra.[19][20] The large aspiny cholinergic interneurons themselves are affected by dopamine through D5 dopamine receptors.[21] Dopamine also directly controls communication between cholinergic interneurons.[22][23]
  • There are many types of GABAergic interneurons.[24] The best known are parvalbumin expressing interneurons, also known as fast-spiking interneurons, which participate in powerful feedforward inhibition of principal neurons.[25] Also, there are GABAergic interneurons that express tyrosine hydroxylase,[26] somatostatin, nitric oxide synthase and neuropeptide-y. Recently, two types of neuropeptide-y expressing GABAergic interneurons have been described in detail,[27] one of which translates synchronous activity of cholinergic interneurons into inhibition of principal neurons.[28] These neurons of the striatum are not distributed evenly.[24]

There are two regions of neurogenesis in the brain – the subventricular zone (SVZ) in the lateral ventricles, and the dentate gyrus in the hippocampal formation. Neuroblasts that form in the lateral ventricle adjacent to the striatum, integrate in the striatum.[29][30] This has been noted in the human striatum following an ischemic stroke. Injury caused to the striatum stimulates the migration of neuroblasts from the SVZ, to the striatum, where they differentiate into adult neurons.[31] The normal passage of SVZ neuroblasts is to the olfactory bulb but this traffic is diverted to the striatum after an ischemic stroke. However, few of the new developed neurons survive.[32]

Inputs

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Simplified diagram of frontal cortex to striatum to thalamus pathways – frontostriatal circuit
Overview of the main circuits of the basal ganglia. The striatum is shown in blue. Picture shows 2 coronal slices that have been superimposed to include the involved basal ganglia structures. + and – signs at the point of the arrows indicate respectively whether the pathway is excitatory or inhibitory in effect. Green arrows refer to excitatory glutamatergic pathways, red arrows refer to inhibitory GABAergic pathways and turquoise arrows refer to dopaminergic pathways that are excitatory on the direct pathway and inhibitory on the indirect pathway.

The largest connection is from the cortex, in terms of cell axons. Many parts of the neocortex innervate the dorsal striatum. The cortical pyramidal neurons projecting to the striatum are located in layers II-VI, with the most dense projections come from layer V.[33] They end mainly on the dendritic spines of the spiny neurons. They are glutamatergic, exciting striatal neurons.

The striatum is seen as having its own internal microcircuitry.[34] The ventral striatum receives direct input from multiple regions in the cerebral cortex and limbic structures such as the amygdala, thalamus, and hippocampus, as well as the entorhinal cortex and the inferior temporal gyrus.[35] Its primary input is to the basal ganglia system. Additionally, the mesolimbic pathway projects from the ventral tegmental area to the nucleus accumbens of the ventral striatum.[36]

Another well-known afferent is the nigrostriatal connection arising from the neurons of the substantia nigra pars compacta. While cortical axons synapse mainly on spine heads of spiny neurons, nigral axons synapse mainly on spine shafts. In primates, the thalamostriatal afferent comes from the central median-parafascicular complex of the thalamus (see primate basal ganglia system). This afferent is glutamatergic. The participation of truly intralaminar neurons is much more limited. The striatum also receives afferents from other elements of the basal ganglia such as the subthalamic nucleus (glutamatergic) or the external globus pallidus (GABAergic).

Targets

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Further information: Medium spiny neuron

The primary outputs of the ventral striatum project to the ventral pallidum, then the medial dorsal nucleus of the thalamus, which is part of the frontostriatal circuit. Additionally, the ventral striatum projects to the globus pallidus, and substantia nigra pars reticulata. Some of its other outputs include projections to the extended amygdala, lateral hypothalamus, and pedunculopontine nucleus.[37]

Striatal outputs from both the dorsal and ventral components are primarily composed of medium spiny neurons (MSNs), a type of projection neuron, which have two primary phenotypes: "indirect" MSNs that express D2-like receptors and "direct" MSNs that express D1-like receptors.[2][4]

The main nucleus of the basal ganglia is the striatum which projects directly to the globus pallidus via a pathway of striatopallidal fibers.[38] The striato-pallidal pathway has a whitish appearance due to the myelinated fibers. This projection comprises successively the external globus pallidus (GPe), the internal globus pallidus (GPi), the pars compacta of the substantia nigra (SNc), and the pars reticulata of substantia nigra (SNr). The neurons of this projection are inhibited by GABAergic synapses from the dorsal striatum. Among these targets, the GPe does not send axons outside the system. Others send axons to the superior colliculus. Two others comprise the output to the thalamus, forming two separate channels: one through the internal segment of the globus pallidus to the ventral oralis nuclei of the thalamus and from there to the cortical supplementary motor area and another through the substantia nigra to the ventral anterior nuclei of the thalamus and from there to the frontal cortex and the occulomotor cortex.

Blood supply

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Deep penetrating striate arteries supply blood to the striatum. These arteries include the recurrent artery of Heubner arising from the anterior cerebral artery, and the lenticulostriate arteries arising from the middle cerebral artery.[39]

Function

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The ventral striatum, and the nucleus accumbens in particular, primarily mediates reward, cognition, reinforcement, and motivational salience. By contrast, the dorsal striatum primarily mediates cognition involving motor function, certain executive functions (e.g., inhibitory control and impulsivity), and stimulus-response learning.[2][3][4][40][41] There is a small degree of overlap, as the dorsal striatum is also a component of the reward system that, along with the nucleus accumbens core, mediates the encoding of new motor programs associated with future reward acquisition (e.g., the conditioned motor response to a reward cue).[3][40]

The striatum is also thought to play a role in an at least partially dissociable executive control network for language, applied to both verbal working memory and verbal attention. These models take the form of a frontal-striatal network for language processing.[42] While the striatum is often not included in models of language processing, as most models only include cortical regions, integrative models are becoming more popular in light of imaging studies, lesion studies on aphasic patients, and studies of language disorders concomitant with diseases known to affect the striatum like Parkinson's and Huntington's disease.[43]

Metabotropic dopamine receptors are present both on spiny neurons and on cortical axon terminals. Second messenger cascades triggered by activation of these dopamine receptors can modulate pre- and postsynaptic function, both in the short term and in the long term.[44][45] In humans, the striatum is activated by stimuli associated with reward, but also by aversive, novel,[46] unexpected, or intense stimuli, and cues associated with such events.[47] fMRI evidence suggests that the common property linking these stimuli, to which the striatum is reacting, is salience under the conditions of presentation.[48][49] A number of other brain areas and circuits are also related to reward, such as frontal areas. Functional maps of the striatum reveal interactions with widely distributed regions of the cerebral cortex important to a diverse range of functions.[50]

The interplay between the striatum and the prefrontal cortex is relevant for behavior, particularly adolescent development as proposed by the dual systems model.[51]

Clinical significance

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Parkinson's disease and other movement disorders

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Parkinson's disease results in loss of dopaminergic innervation to the dorsal striatum (and other basal ganglia) and a cascade of consequences. Atrophy of the striatum is also involved in Huntington's disease, and movement disorders such as chorea, choreoathetosis, and dyskinesias.[52] These have also been described as circuit disorders of the basal ganglia.[53]

Addiction

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Overview of reward structures and associated pathways

Addiction, a disorder of the brain's reward system, arises through the overexpression of DeltaFosB (ΔFosB), a transcription factor, in the D1-type medium spiny neurons of the ventral striatum. ΔFosB is an inducible gene which is increasingly expressed in the nucleus accumbens as a result of repeatedly using an addictive drug or overexposure to other addictive stimuli.[54][55]

Schizophrenia spectrum disorders

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The mesolimbic hypothesis of schizophrenia has long emphasized the role of hyperdopaminergia in the mesolimbic pathway, which extends from the ventral tegmental area to the ventral striatum.[56] Abnormally elevated dopaminergic transmission in this pathway has been associated with the emergence of positive symptoms, such as hallucinations and delusions.[57] Most antipsychotic treatments exert their effects by reducing dopamine binding to receptors in this region.[58] More recent evidence, however, suggests that the pathway from the substantia nigra to the dorsal striatum may also play a significant role in the pathophysiology of schizophrenia.[59] This has led to the development of the mesostriatal hypothesis, which expands the focus beyond the ventral striatum to include dopaminergic dysfunction in the dorsal components of the striatum and could help accounting for the negative and cognitive symptoms.[60]

Bipolar disorder

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An association has been observed between striatal expression of variants of the PDE10A gene and some bipolar I disorder patients. Variants of other genes, DISC1 and GNAS, have been associated with bipolar II disorder.[61]

Autism spectrum disorder

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Autism spectrum disorder (ASD) is characterized by cognitive inflexibility and poor understanding of social systems. This inflexible behavior originates in defects in the prefrontal cortex as well as the striatal circuits.[62] The defects in the striatum seem to specifically contribute to the motor, social and communication impairments seen in ASD patients. In mice which have an ASD-like phenotype induced via the overexpression of the eukaryotic initiation of translation factor 4E, it has been shown that these defects seem to stem from the reduced ability to store and process information in the striatum, which leads to the difficulty seen in forming new motor patterns, as well as disengaging from existing ones.[63]

Dysfunction

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Dysfunction in the ventral striatum can lead to a variety of disorders, most notably depression and obsessive-compulsive disorder. Because of its involvement in reward pathways, the ventral striatum has also been implicated in playing a critical role in addiction. It has been well established that the ventral striatum is strongly involved in mediating the reinforcing effects of drugs, especially stimulants, through dopaminergic stimulation.[64]

Language disorders

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Lesions to the striatum have been associated with deficits in speech production and comprehension. While striatal damage can impact all levels of language, damage can broadly be characterized as affecting the ability to manipulate linguistic units and rules, resulting in the promotion of default linguistic forms in conflicting situations in which selection, inhibition, and monitoring load is increased.[65] Two subregions of the striatum have been shown to be particularly important in language: the caudate nucleus and left putamen. Lesions localized to the caudate nucleus, as well as direct electrical stimulation, can result in lexical paraphasias and perservations (continuations of an utterance after the stimulus has ceased), which is associated with inhibited executive control, in the sense that executive control allows for the selection of the best choice among competing alternatives.[66] Stimulation of the putamen results in the inhibition of articulatory sequences and the inability to initiate motor speech commands.[67][68]

History

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In the seventeenth and eighteenth centuries, the term corpus striatum was used to designate many distinct, deep, infracortical elements of the[which?] hemisphere.[69] Etymologically, it is derived from (Latin) striatus [70] = "grooved, striated" and the English striated = having parallel lines or grooves on the surface.[71] In 1876 David Ferrier contributed decades of research to the subject; concluding that the corpus striatum was vital in the "organization and generation of voluntary movement".[72][73][74][75][76] In 1941, Cécile and Oskar Vogt simplified the nomenclature by proposing the term striatum for all elements in the basal ganglia built with striatal elements: the caudate nucleus, the putamen, and the fundus striati,[77] which is the ventral part linking the two preceding together ventrally to the inferior part of the internal capsule.

The term neostriatum was coined by comparative anatomists comparing the subcortical structures between vertebrates, because it was thought to be a phylogenetically newer section of the corpus striatum. The term is still used by some sources, including Medical Subject Headings.[78]

Other animals

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In birds the term used was the paleostriatum augmentatum, while in the new avian terminology listing (as of 2002) for neostriatum this has been changed to the nidopallium.[79]

In non-primate species, the islands of Calleja are included in the ventral striatum.[11]

See also

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Additional images

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  • Striatum highlighted in green on coronal T1 MRI images
    Striatum highlighted in green on coronal T1 MRI images
  • Striatum highlighted in green on sagittal T1 MRI images
    Striatum highlighted in green on sagittal T1 MRI images
  • Striatum highlighted in green on transversal T1 MRI images
    Striatum highlighted in green on transversal T1 MRI images

References

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[edit]
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Striatum

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The striatum is a key subcortical nucleus of the in the mammalian , comprising the dorsal striatum ( and ) and the ventral striatum (primarily the ), which collectively serve as the primary input region for processing cortical and thalamic signals to regulate voluntary movement, reward processing, and habit formation. Located deep within the cerebral hemispheres, the striatum receives dense projections from nearly all regions of the , as well as dopaminergic inputs from the and , enabling it to integrate sensory, motor, and motivational information. Its medium spiny neurons, which constitute about 95% of its neuronal population, form the core of its circuitry, modulating output to downstream structures like the and through direct and indirect pathways that facilitate action selection and suppression. Functionally, the dorsal striatum is predominantly involved in motor planning, procedural learning, and the execution of habitual behaviors, transforming cortical commands into refined actions via loops with the and . In contrast, the ventral striatum plays a central role in reward anticipation, motivation, and emotional processing, contributing to and decision-making through connections with the and . Dysfunctions in striatal circuitry are implicated in various neurological and psychiatric disorders, including , , , and , underscoring its evolutionary conservation across vertebrates for . Recent and optogenetic studies have further elucidated its compartmental into striosomes and matrix zones, which differentially influence and signaling to fine-tune responses to environmental cues.

Anatomy

Location and Divisions

The striatum forms a principal component of the , positioned deep within the as a subcortical structure beneath the , immediately adjacent to the and the . It is anatomically divided into the dorsal striatum, consisting of the and , and the ventral striatum, encompassing the and ; the dorsal portion occupies a more superior and lateral position, while the ventral division lies inferiorly at the base of the , with the serving as the primary boundary separating the caudate from the . The adopts a distinctive C-shaped morphology, featuring an anterior head, elongated body along the lateral ventricular wall, and tapering tail that curves posteriorly, whereas the presents a compact, lens-shaped form nestled lateral to the and . In human adults, the measures approximately 6-7 cm³ per hemisphere, with the exhibiting a comparable size of around 6-7 cm³ per hemisphere, varying by sex and population. These major divisions of the striatum demonstrate strong evolutionary conservation across mammalian , maintaining similar gross anatomical organization from to .

Cellular Composition

The striatum's neuronal population is predominantly composed of medium spiny neurons (MSNs), which account for 75-90% of all striatal neurons in humans and serve as the primary projection neurons. These MSNs are and can be subdivided into two major subtypes based on their expression of : those expressing D1-like receptors (D1-MSNs), which are part of the direct pathway, and those expressing D2-like receptors (D2-MSNs), which belong to the indirect pathway. This dichotomy underlies the striatum's role in modulating motor and reward-related functions through differential responses to dopaminergic inputs. The remaining 10-25% of striatal neurons consist of diverse that provide local inhibition and modulation. These include cholinergic interneurons, which comprise about 1-2% of the total neuronal population and are tonically active, releasing to regulate MSN excitability. interneurons form the majority of this subclass, encompassing fast-spiking interneurons (FSIs) expressing parvalbumin (approximately 1-3% of neurons), which deliver strong, rapid inhibition to , and low-threshold spiking interneurons (LTSIs) co-expressing and (about 1-2% of neurons), which provide more prolonged inhibitory control. Additionally, calretinin-positive interneurons, a major type (roughly 5-10% of neurons), contribute to fine-tuned local circuitry. Recent transcriptomic studies have identified eight main classes and fourteen subclasses of striatal , highlighting greater diversity than in . Beyond neurons, glial cells form a critical supportive component of the striatal architecture, comprising a substantial portion of the total cellular population—astrocytes alone estimated at 20-40% of cells overall, with similar representation in the striatum. in the striatum exhibit region-specific molecular profiles, such as elevated μ-crystallin expression in ventral areas, and play key roles in maintaining by regulating extracellular ion balance, providing metabolic substrates like lactate to energy-demanding MSNs, and modulating synaptic transmission through calcium-dependent gliotransmitter release. Each striatal typically contacts around 11 MSNs and encompasses thousands of synapses, facilitating bidirectional neuron-glia interactions that influence circuit dynamics. , responsible for myelinating striatal axons, support efficient signal propagation and provide trophic factors to neurons, ensuring structural integrity and responding to pathological changes by promoting remyelination. The striatum is further organized into neurochemically distinct compartments: striosomes and the surrounding matrix, which together define its functional mosaic. Striosomes occupy 10-15% of the striatal volume, appearing as irregular patches enriched in mu-opioid receptors and , with lower levels compared to the matrix. This compartmentalization influences cellular distribution, as striosomes contain a higher density of opioid-sensitive MSNs, while the matrix—making up the bulk of the striatum—hosts more uniformly distributed projection neurons integrated with broader cortical inputs.

Connectivity

The striatum serves as a key hub in circuitry, receiving convergent afferent inputs that integrate sensory, motor, and cognitive information. The predominant excitatory afferents are projections from the , forming dense corticostriatal pathways that exhibit topographic organization, with prefrontal areas targeting the ventral striatum and sensorimotor cortices innervating the dorsal regions; these inputs synapse primarily onto spines of medium spiny neurons (MSNs), selectively modulating direct and indirect pathway neurons based on cortical layer and region specificity. afferents originate from the (SNc), which projects via the to the dorsal striatum to regulate motor functions, and from the (VTA), which innervates the ventral striatum through the to influence reward processing. Serotonergic inputs arise from neurons in the dorsal and median , providing modulatory projections that interact with dopaminergic terminals to balance striatal excitability and behavioral flexibility. Efferent outputs from the striatum are predominantly and arise from two main populations of MSNs, which comprise over 90% of striatal neurons and express either D1 or D2 . MSNs of the direct pathway, expressing D1 receptors, project monosynaptically to the internal segment of the (GPi) and the pars reticulata (SNr), disinhibiting thalamocortical circuits to facilitate movement initiation. In contrast, MSNs of the indirect pathway, expressing D2 receptors, target the external segment of the (GPe), which in turn influences the subthalamic nucleus and indirect pathway targets, thereby suppressing unwanted movements through increased output inhibition. These afferent and efferent connections integrate into parallel cortico-striato-thalamo-cortical loops that segregate functional domains: the sensorimotor loop involves projections from primary motor and somatosensory cortices through the to motor ; the associative loop links prefrontal and parietal cortices via the caudate to cognitive thalamic nuclei; and the limbic loop connects orbitofrontal and anterior cingulate cortices through the to limbic thalamic regions, enabling coordinated processing across behavioral modalities. Local striatal circuitry further refines through recurrent axonal collaterals among s, which mediate to sharpen response selectivity, and through modulatory actions of , including tonically active interneurons that regulate MSN excitability via muscarinic and nicotinic receptors, as well as fast-spiking parvalbumin-positive interneurons that provide perisomatic inhibition.

Vascular Supply

The striatum receives its primary arterial blood supply from the lenticulostriate arteries, which are small perforating branches arising from the M1 segment of the (MCA). These vessels, numbering typically between 2 and 12 with diameters ranging from 80 to 1,400 μm (averaging 100-200 μm), penetrate the to irrigate the majority of the dorsal striatum, including the and much of the . The lateral lenticulostriate arteries predominantly supply the and lateral aspects of the caudate, while the medial branches target the medial caudate and adjacent structures; limited anastomoses exist between these territories, providing some redundancy but overall sparse collateral circulation. Additional supply to specific regions comes from the recurrent artery of Heubner, a medial striate artery originating from the anterior cerebral artery (ACA), which vascularizes the anterior head and body of the caudate nucleus as well as the anterior inferior internal capsule. The posterior portions of the striatum, particularly the tail of the caudate and lower globus pallidus, are supplied by branches of the anterior choroidal artery, which arises from the internal carotid artery and courses along the optic tract. These complementary arterial inputs ensure comprehensive coverage of the striatal subregions, though the small caliber of the perforators limits robust interconnections. Venous drainage of the striatum primarily occurs via the thalamostriate vein (also known as the vena terminalis), which collects blood from the and adjacent thalamic regions before joining the internal cerebral vein to form the of Galen. Superior lenticular veins from the and converge into this system, facilitating efficient outflow toward the dural sinuses. The deep venous architecture mirrors the arterial end-artery pattern, contributing to regional vulnerability. Due to the small vessel diameters and lack of significant collaterals, the striatal vascular territory is particularly susceptible to lacunar infarcts from occlusion of single , often resulting from or microatheroma in small vessel disease. Such infarcts, typically under 15 mm in diameter, can disrupt striatal without widespread hemispheric involvement.

Development

Embryonic Origins

The striatum primarily derives from progenitor cells in the lateral ganglionic eminence (LGE), a transient proliferative structure in the ventral telencephalon that emerges during early embryonic development. In humans, the LGE forms around gestational weeks 5-6, coinciding with the initial patterning of the subpallium, while in mice, the LGE becomes morphologically distinct by embryonic day (E) 11, marking the onset of striatal specification. Initial in the LGE begins by E12.5 in mice, equivalent to approximately week 7 of human , generating the first cohorts of striatal projection neurons. Specification of LGE progenitors relies on critical transcription factors that orchestrate regional identity and neuronal fate. The gene Gsh2 plays a pivotal role in progenitor proliferation and patterning within the LGE, ensuring proper histogenesis of striatal and olfactory bulb structures; mutants exhibit severe reductions in LGE-derived neurons. Similarly, Dlx1 and Dlx2 are essential for promoting the phenotype in nascent striatal neurons, particularly medium spiny neurons (MSNs), by regulating downstream s involved in differentiation and migration. These factors act in a hierarchical manner, with Gsh2 upstream influencing Dlx expression to refine ventral telencephalic identities. Following their generation in the LGE ventricular zone, MSNs migrate to form the nascent striatum through a of radial and tangential pathways. Radial migration predominates, with newborn neurons ascending along radial glial scaffolds from the LGE to populate the striatal mantle; this process establishes the basic laminar organization. Tangential migration, involving lateral movements within the intermediate zone, contributes to the intermixing of MSN subtypes, such as direct- and indirect-pathway neurons, enhancing striatal mosaicism. By E15.5 in mice, these migratory dynamics culminate in the compartmentalization of the striatum into striosome (patch) and matrix domains, reflecting differential birth dates and molecular signatures of progenitors.

Postnatal Maturation

The postnatal maturation of the striatum involves extensive synaptic refinement, system development, and integration of environmental influences to establish functional circuits essential for motor, reward, and cognitive processes. in the human striatum, as in other regions, peaks during the first two years of life, with rapid formation of excitatory and inhibitory synapses on medium spiny neurons driven by inputs from the cortex and . This overproduction of synapses reaches a maximum in early postnatal life before stabilizing through selective elimination. then predominates during , reducing connectivity in striatal regions to enhance circuit efficiency and specificity, a process guided by activity-dependent mechanisms. The system undergoes critical postnatal tuning, with midbrain-derived innervation of the striatum largely established prenatally by mid-gestation, followed by functional maturation involving increasing release and receptor , particularly D1 and D2 subtypes on direct and indirect pathway neurons, which refines circuit tuning for reward processing and . In , neurotransmission ramps up from the first to third postnatal week, preceding spiny projection maturation and influencing synaptic strengthening in the direct pathway. These changes continue through in humans, with striatal signaling specializing regionally to support behavioral transitions. Experience-dependent plasticity plays a key role in shaping corticostriatal connections during early postnatal periods, where sensory from the environment modulate synaptic strength and dendritic arborization in striatal neurons. Early sensory experiences, such as tactile or auditory stimuli, drive at corticostriatal synapses, refining projections from sensorimotor and associative cortices to match behavioral demands. This plasticity is particularly pronounced in the first few years, when thalamic and cortical afferents integrate sensory information to stabilize striatal maps. Adolescence represents a for striatal maturation, particularly for formation, as enhanced signaling shifts behaviors from goal-directed to actions via strengthened indirect pathway circuits. During this window, typically ages 10-20, and myelination optimize corticostriatal loops, making the system more responsive to . differences emerge, with females exhibiting earlier striatal volume peaks (around 12 years) compared to males (around 15 years), potentially contributing to divergent timelines in consolidation and reward sensitivity.

Functions

Motor Control

The striatum plays a pivotal role in through its integration into the basal ganglia-thalamocortical circuits, where it modulates the initiation and execution of voluntary movements. Medium spiny neurons (MSNs) in the striatum, which constitute the primary output neurons, are segregated into two major pathways based on their expression and projections. This organization allows the striatum to balance facilitation and suppression of motor actions, ensuring precise action selection and suppression of competing movements. The direct pathway, comprising D1 receptor-expressing MSNs (D1-MSNs), promotes movement by projecting directly to the internal segment of the (GPi) and pars reticulata (SNr), the output nuclei of the . Activation of D1-MSNs inhibits these output structures, leading to disinhibition of thalamocortical projections to motor areas in the cortex, thereby facilitating the selected movement. This pathway is essential for the initiation and vigor of voluntary actions, as demonstrated in optogenetic studies where selective stimulation of D1-MSNs accelerates motor responses and enhances movement execution. In contrast, the indirect pathway, formed by D2 receptor-expressing MSNs (D2-MSNs), inhibits inappropriate or unwanted movements by projecting to the external segment of the (GPe). D2-MSN activation inhibits the GPe, leading to disinhibition of the subthalamic nucleus (STN), which in turn excites the GPi/SNr, ultimately increasing inhibitory output from the GPi/SNr to the and suppressing motor activity. This pathway refines by preventing extraneous actions, with electrophysiological evidence showing that D2-MSN activity correlates with the suppression of competing motor programs during task performance. A key aspect of striatal motor function is the sensorimotor loop, which integrates inputs from cortical motor and somatosensory areas primarily through the , the dorsal striatal region dominant in motor processing. This loop allows the striatum to process sensory feedback alongside motor commands, enabling adaptive adjustments during movement execution, such as in sequential tasks where putaminal activity modulates the scaling of motor output based on sensory cues. The striatum's role in action selection is captured by the Go/No-Go model, in which the direct pathway signals "Go" for desired actions and the indirect pathway signals "No-Go" to veto alternatives. inputs from the bias this selection by exciting D1-MSNs and inhibiting D2-MSNs, thereby promoting the execution of contextually appropriate movements while suppressing others, as evidenced in computational models and recordings during tasks.

Reward Processing

The ventral striatum, particularly the , serves as a core structure for distinguishing between hedonic "liking"—the sensory pleasure derived from rewards—and motivational "wanting"—the incentive drive to pursue them. Hedonic hotspots, localized in the medial shell of the , are discrete sites where μ-opioid receptor stimulation amplifies the affective "liking" reactions to palatable rewards, such as enhanced facial expressions of pleasure in response to in animal models. These hotspots interact with similar opioid-sensitive regions in the to generate the core hedonic impact of rewards. In contrast, "wanting" is primarily driven by mesolimbic projections to the nucleus accumbens shell, which enhance the incentive salience of reward cues, motivating approach behaviors without necessarily altering the sensory pleasure itself. Dopamine signaling in the striatum is pivotal for reward prediction and learning, with phasic bursts from neurons encoding reward prediction errors (RPEs) that update value expectations. These RPEs reflect discrepancies between anticipated and actual rewards, as demonstrated in seminal electrophysiological recordings where neurons respond tonically to unexpected rewards and phasically to cues predicting them after learning. This is formalized in temporal difference (TD) learning models, where the RPE is computed as δ=r+γV(s′)−V(s)\delta = r + \gamma V(s') - V(s) with δ\delta denoting the prediction error, rr the immediate reward, γ\gamma the discount factor for future rewards, V(s)V(s) the value of the current state ss, and V(s′)V(s') the value of the next state s′s'. In the striatum, these dopamine signals arrive via the nigrostriatal and mesolimbic pathways, enabling medium spiny neurons—primarily expressing D1 or D2 dopamine receptors—to adjust synaptic weights and refine reward associations. The striatum integrates reward information through corticostriatal-limbic circuits, where inputs from the and (OFC) contribute to value encoding. Basolateral amygdala projections convey emotional and associative value signals to the ventral striatum, facilitating the representation of reward outcomes in contexts. Similarly, OFC inputs provide abstract representations of reward magnitude and probability, which ventral striatal neurons encode as the specific value of selected actions during goal-directed choices. This convergence allows the striatum to compute integrated value signals that guide . Through TD learning mechanisms, the striatum updates reward expectations based on outcome discrepancies, with dopamine RPEs serving as the primary teaching signal. Ventral striatal circuits act as a critic in , propagating TD errors to adjust predictive values over time, as evidenced by neural activity patterns that shift from immediate rewards to anticipatory cues during Pavlovian conditioning. This iterative process enables the striatum to optimize by refining predictions of future rewards across extended timescales.

Cognitive and Habitual Behaviors

The dorsal striatum plays a pivotal role in distinguishing between goal-directed actions, which are flexible and outcome-sensitive, and habitual actions, which are automatic and stimulus-response driven. In humans and , the dorsomedial striatum, including the , supports goal-directed behavior by integrating action-outcome contingencies, allowing for adaptive based on changing environmental rewards. In contrast, the dorsolateral striatum, encompassing the , facilitates the formation of habits through stimulus-response associations, enabling efficient, overlearned behaviors that operate independently of outcomes. This functional dissociation is evidenced by studies showing caudate activation during tasks requiring sensitivity to action values, while putamen activity increases with habitual responding. The associative striatum, particularly the caudate, forms part of a cortico-striatal loop that integrates with the to underpin and . This loop enables the maintenance and manipulation of goal-relevant information, supporting in complex decision-making scenarios. Projections from the to the caudate modulate and , allowing individuals to prioritize and sequence cognitive operations for prospective . Functional MRI evidence demonstrates that disruptions in this prefrontal-striatal connectivity impair performance, highlighting the striatum's role in bridging sensory inputs with executive outputs. In procedural learning, the dorsolateral striatum contributes to the chunking of action s, transforming discrete movements into fluid, integrated behaviors. This process involves grouping individual actions into larger units, which facilitates the efficient execution of learned routines, such as motor skills or cognitive procedures. Electrophysiological recordings in reveal that dorsolateral striatal neurons encode sequence boundaries and transitions, promoting the consolidation of chunks during . Human studies corroborate this, showing increased activity when participants automate sequential tasks, reducing for habitual performance. Normal variations in striatal function contribute to individual differences in compulsive tendencies, akin to milder forms of OCD-like behaviors in healthy populations. Stronger habitual control via the dorsolateral striatum correlates with repetitive checking or ordering behaviors in non-clinical samples, reflecting an adaptive but sometimes rigid reliance on routines. These variations are linked to transdiagnostic traits of compulsivity, where enhanced striatal habit circuits predict greater persistence in goal-irrelevant actions under uncertainty. Such findings suggest that the striatum's balance between flexibility and automation underlies subclinical compulsions, without implying pathology.

Clinical Significance

Movement Disorders

The striatum plays a central role in , where dysfunction in its neural circuits leads to characteristic motor impairments. In , progressive degeneration of neurons in the pars compacta results in depletion primarily in the dorsal striatum, which underlies key motor symptoms such as bradykinesia and rigidity. This depletion disrupts the balance between the direct and indirect pathways in the , reducing excitatory drive to thalamocortical motor circuits and contributing to hypokinetic features. Additionally, aggregates and dystrophic neurites are observed in the striatum, particularly in medium spiny neurons (MSNs), exacerbating neuronal dysfunction and synaptic loss in advanced stages. Huntington's disease, an autosomal dominant neurodegenerative disorder, arises from an expanded CAG trinucleotide repeat in the (HTT) on , leading to a toxic gain-of-function in the mutant huntingtin protein. This mutation causes progressive striatal atrophy, particularly in the and , manifesting as hyperkinetic choreiform movements due to impaired motor inhibition. Neuropathologically, there is selective vulnerability and loss of MSNs, with those in the indirect pathway (expressing D2 and projecting to the externa) degenerating earlier and more severely than direct pathway MSNs, resulting in disinhibition of thalamocortical outputs and involuntary movements. Dystonia involves abnormal sustained muscle contractions leading to twisted postures, often linked to striatal circuit imbalances. In primary dystonias, such as DYT1-TOR1A, a GAG deletion in the TOR1A gene encoding torsinA disrupts and function, altering the direct-indirect pathway equilibrium in the striatum toward excessive direct pathway activity and reduced surround inhibition. Similarly, Tourette's syndrome features tics arising from striatal hyperactivity, with genetic factors contributing to an imbalance favoring the direct pathway over the indirect, as evidenced by reduced striatal density and dysregulated modulation in affected individuals. Therapeutic interventions targeting striatal outputs have shown efficacy in managing these disorders. (DBS) of the subthalamic nucleus normalizes excessive beta oscillations and modulates downstream circuits, including striatal projections, thereby alleviating bradykinesia and rigidity in by enhancing thalamocortical drive without directly stimulating the striatum. In and Huntington's, STN-DBS similarly influences striatal outflow via the hyperdirect pathway, reducing hyperkinetic symptoms by restoring inhibitory balance in the indirect pathway.

Neuropsychiatric Disorders

The striatum plays a critical role in the of several neuropsychiatric disorders, particularly through its involvement in signaling, reward processing, and cortico-striatal circuits that modulate and emotion. In , excessive release in the ventral striatum, part of the , is implicated in the emergence of positive symptoms such as delusions and hallucinations, as evidenced by studies showing elevated striatal synthesis capacity in patients during acute psychotic episodes. This hyperdopaminergia disrupts the balance of striatal subregions, leading to aberrant salience attribution where neutral stimuli are perceived as overly significant. Conversely, negative symptoms like and blunted affect are associated with hypofrontality in prefrontal-striatal circuits, particularly involving the associative striatum (dorsomedial caudate and ), where reduced modulation impairs executive function and motivation, as demonstrated in of medicated and unmedicated patients. In bipolar disorder, striatal dysregulation manifests differently across mood states, with hyperactivity in the ventral striatum during manic phases contributing to elevated reward sensitivity and impulsivity. (fMRI) studies reveal increased ventral striatal activation in response to reward cues in individuals with experiencing , correlating with symptom severity on scales like the Young Mania Rating Scale. This hyperactivity may stem from enhanced transmission in the , exacerbating goal-directed behaviors and risk-taking. Structurally, volumetric reductions in the are consistently observed in bipolar patients, independent of mood state, with meta-analyses indicating smaller caudate volumes bilaterally compared to healthy controls, potentially reflecting trait-related neurodevelopmental alterations that predispose to mood instability. Autism spectrum disorder (ASD) involves early striatal abnormalities that align with core behavioral features, including repetitive behaviors. Longitudinal MRI studies show caudate nucleus enlargement in toddlers with ASD as young as 2-3 years old, with this volumetric increase persisting and correlating with the severity of restricted and repetitive behaviors (RRBs) measured by the Repetitive Behavior Scale-Revised. Such enlargement, often disproportionate to overall brain growth, implicates disrupted striatal development in ritualistic patterns. Furthermore, altered corticostriatal connectivity underlies these traits, with fMRI evidence of precocious maturation and hyperactivity in circuits linking the to the dorsal striatum in preschool-aged children with ASD, leading to inflexible habit formation and sensory sensitivities. Recent research since 2020 highlights the striatum's role in deficits across neuropsychiatric conditions, particularly through disruptions in -orbitofrontal cortex connectivity. In and ASD, reduced functional coupling between the and orbitofrontal regions impairs social reward processing, as shown in resting-state fMRI studies where lower connectivity predicts deficits in theory of mind tasks and social withdrawal. Similar orbitofrontal-striatal dysconnectivity in during euthymic phases contributes to impaired , with volumetric reductions in the mediating social functioning impairments in large cohort analyses. These findings underscore shared striatal mechanisms in social deficits, suggesting potential targets for circuit-based interventions like .

Addiction and Reward Dysregulation

The striatum, particularly its ventral portion encompassing the , plays a pivotal role in through dysregulation of the mesolimbic pathway. Drugs of abuse, such as , hijack this pathway by blocking transporters, thereby elevating extracellular levels in the and producing intense . This acute surge reinforces drug-seeking behavior via enhanced reward signaling, but chronic exposure leads to tolerance, where higher doses are required to achieve the same effect due to diminished responsiveness. Withdrawal from these substances then manifests as and , driven by depleted transmission in the same circuit, perpetuating the addiction cycle. In the progression of addiction, there is a notable shift from ventral to dorsal striatum involvement, transforming initially goal-directed use into compulsive, habitual seeking. Early consumption is mediated by the ventral striatum's sensitivity to reward cues, but with prolonged use, control transfers to the dorsal striatum, where inflexible habits dominate behavior despite negative consequences. This transition promotes persistent -seeking even in the face of adverse outcomes, as dorsal striatal circuits prioritize automatic responses over flexible . Key neuroadaptations in the striatum underlie these changes, including downregulation of D2 receptors, which reduces over reward circuits and heightens vulnerability to . In medium spiny neurons, epigenetic modifications such as the accumulation of ΔFosB—a stable induced by repeated drug exposure—persistently alter to enhance sensitivity to drug-related cues and reinforce addictive behaviors. This ΔFosB buildup occurs selectively in D1-type medium spiny neurons of the , driving long-term plasticity that sustains . Behavioral addictions, such as pathological , exhibit analogous dysregulation without pharmacological agents, characterized by ventral striatal to reward and cues. In gamblers, this manifests as exaggerated responses in the during monetary wins or near-misses, mirroring substance-induced changes and fostering compulsive engagement. Such disrupts normal reward prediction error signaling in the striatum, amplifying the motivational pull of the .

History and Comparative Aspects

Historical Discoveries

The striatum, a key component of the , was first described in the by English physician and anatomist in his seminal work Cerebri anatome published in 1664, where he referred to it as the "corpus striatum" due to its striped appearance from myelinated fibers. Willis's detailed illustrations and observations laid foundational groundwork for understanding subcortical structures, emphasizing their role in neural connectivity. In the late , French anatomist Félix Vicq d'Azyr advanced this knowledge through his Traité d'anatomie et de physiologie (1786), in which he distinguished and named the and as separate components of the striatum, providing clearer delineations via anatomical plates. This nomenclature clarified the striatum's internal organization, facilitating subsequent studies on its boundaries and relations to surrounding tracts. The 19th century saw further integration of the striatum into broader concepts, with Austrian neurologist Theodor Meynert contributing to the integration of the striatum into broader concepts in the . Concurrently, British physician James Parkinson's 1817 essay An Essay on the Shaking Palsy provided the earliest clinical description of what became known as , noting involuntary tremors and rigidity later associated with striatal dysfunction, though without direct anatomical correlation at the time. The 20th century brought neurochemical insights, particularly through Swedish pharmacologist Arvid Carlsson's 1950s experiments demonstrating as a in the , including its high concentrations in the striatum, which earned him the in or in 2000. This discovery illuminated the nigrostriatal dopamine pathway's importance in . Building on this, in the 1980s, researchers Roger Albin, Anne Young, and Mahlon DeLong proposed the direct and indirect pathway model of circuitry, positing that striatal medium spiny neurons modulate thalamic output via D1- and D2- receptor pathways to facilitate or inhibit movement. From the 1990s onward, (fMRI) advancements enabled non-invasive mapping of striatal activity, revealing its functional subdivisions such as sensorimotor, associative, and limbic regions through task-based and resting-state studies. These techniques confirmed heterogeneous activation patterns, linking ventral striatum to reward and dorsal regions to , thus refining historical anatomical views with dynamic evidence. In the 2010s, optogenetic studies validated the direct and indirect pathway model across species, while as of 2025, advanced neuroimaging techniques continue to refine striatal functional mapping.

Striatum in Non-Human Animals

The striatum exhibits a high degree of homology across vertebrates, serving as a core component of the circuitry involved in action selection and . This conservation is evident from lampreys to mammals, where the striatum receives inputs from pallial (cortical-like) structures and projects to pallidal regions, maintaining fundamental topological organization despite variations in brain size and complexity. In non-mammalian vertebrates such as fish, the , including striatal analogs, facilitate basic action selection during behaviors like prey capture and escape responses, as demonstrated in models where optogenetic manipulation of striatal pathways modulates decision-making in dynamic environments. Similarly, in avian species like songbirds, the striatum's analog—known as Area X within the anterior pathway—plays a critical role in vocal learning, integrating sensory feedback to refine song production through mechanisms akin to mammalian reward processing. Evolutionary trends show increased striatal compartmentalization in mammals, with distinct striosome and matrix domains emerging alongside cortical expansion to support more sophisticated behavioral integration. This compartmentalization, which emerges in mammals alongside the phylogenetic development of the cerebral cortex, allows for segregated processing of motivational and sensorimotor signals, enhancing adaptive responses. In rodents, a key model for striatal research, the nucleus accumbens shell within the ventral striatum is prominently involved in reward processing, encoding hedonic value and motivating approach behaviors; optogenetic studies from the 2010s have elucidated direct and indirect pathway dynamics, revealing how D1- and D2-receptor expressing medium spiny neurons differentially gate reward-seeking versus aversion. These rodent models highlight the striatum's role in habit formation and reinforcement learning, with the shell's medial-lateral gradients tuning sensitivity to natural and drug rewards. Comparative analyses reveal expansions in the striatum across relative to , particularly in associative domains linked to cognitive functions. While exhibit a more compact dorsomedial associative striatum for prelimbic cortical integration, display proportionally larger caudate and regions, supporting enhanced executive control and ; these human-specific enlargements build upon conserved blueprints.

References

  1. https://pmc.ncbi.nlm.nih.gov/articles/PMC3543080/
  2. https://www.sciencedirect.com/science/article/abs/pii/S0166223620302496
  3. https://www.frontiersin.org/journals/systems-neuroscience/articles/10.3389/fnsys.2023.1242929/full
  4. https://www.annualreviews.org/content/journals/10.1146/annurev.neuro.051508.135422
  5. https://pmc.ncbi.nlm.nih.gov/articles/PMC4526748/
  6. https://www.ncbi.nlm.nih.gov/books/NBK92777/
  7. https://www.frontiersin.org/journals/neuroscience/articles/10.3389/fnins.2013.00233/pdf
  8. https://www.biorxiv.org/content/10.1101/2024.12.13.628392v1.full.pdf
  9. https://www.ncbi.nlm.nih.gov/books/NBK537141/
  10. https://synapse.koreamed.org/articles/1039204
  11. https://pmc.ncbi.nlm.nih.gov/articles/PMC3789937/
  12. https://www.sciencedirect.com/science/article/pii/S0960982211005288
  13. https://www.nature.com/articles/s41467-024-50414-w
  14. https://www.nature.com/articles/srep41432
  15. https://pmc.ncbi.nlm.nih.gov/articles/PMC4204445/
  16. https://onlinelibrary.wiley.com/doi/10.1111/nan.12812
  17. https://pmc.ncbi.nlm.nih.gov/articles/PMC6741427/
  18. https://www.nature.com/articles/s41467-023-39046-8
  19. https://pubs.acs.org/doi/10.1021/acschemneuro.6b00333
  20. https://www.jneurosci.org/content/30/44/14610
  21. https://elifesciences.org/articles/19103
  22. https://pmc.ncbi.nlm.nih.gov/articles/PMC11011984/
  23. https://www.sciencedirect.com/science/article/pii/S2211124723002152
  24. https://www.frontiersin.org/journals/integrative-neuroscience/articles/10.3389/fnint.2013.00041/full
  25. https://www.jneurosci.org/content/33/47/18531
  26. https://pmc.ncbi.nlm.nih.gov/articles/PMC9892636/
  27. https://www.nature.com/articles/s41586-021-03993-3
  28. https://www.frontiersin.org/journals/systems-neuroscience/articles/10.3389/fnsys.2016.00104/full
  29. https://pmc.ncbi.nlm.nih.gov/articles/PMC5649445/
  30. https://www.frontiersin.org/journals/synaptic-neuroscience/articles/10.3389/fnsyn.2014.00022/full
  31. https://www.ncbi.nlm.nih.gov/books/NBK541060/
  32. https://pubmed.ncbi.nlm.nih.gov/11301466/
  33. https://nba.uth.tmc.edu/neuroanatomy/l4/Lab04p06_index.html
  34. https://www.ncbi.nlm.nih.gov/books/NBK557407/
  35. https://www.ncbi.nlm.nih.gov/books/NBK557755/
  36. https://pmc.ncbi.nlm.nih.gov/articles/PMC6126264/
  37. https://pubmed.ncbi.nlm.nih.gov/8881556/
  38. https://www.jneurosci.org/content/20/16/6063
  39. https://pmc.ncbi.nlm.nih.gov/articles/PMC8612473/
  40. https://obgyn.onlinelibrary.wiley.com/doi/full/10.1002/uog.26229
  41. https://pubmed.ncbi.nlm.nih.gov/12724834/
  42. https://journals.biologists.com/dev/article/128/23/4769/41483/A-role-for-Gsh1-in-the-developing-striatum-and
  43. https://www.sciencedirect.com/topics/neuroscience/ganglionic-eminence
  44. https://journals.biologists.com/dev/article/149/4/dev200035/274494/Dlx1-2-dependent-expression-of-Meis2-promotes
  45. https://www.jneurosci.org/content/23/1/167
  46. https://www.nature.com/articles/s41467-018-07171-4
  47. https://www.jneurosci.org/content/28/3/622
  48. https://www.pnas.org/doi/10.1073/pnas.2121331119
  49. https://www.frontiersin.org/journals/cellular-neuroscience/articles/10.3389/fncel.2013.00260/full
  50. https://pmc.ncbi.nlm.nih.gov/articles/PMC6602586/
  51. https://www.nature.com/articles/s41467-020-14693-3
  52. https://pmc.ncbi.nlm.nih.gov/articles/PMC5871574/
  53. https://www.jneurosci.org/content/25/49/11279
  54. https://pmc.ncbi.nlm.nih.gov/articles/PMC8930882/
  55. https://pmc.ncbi.nlm.nih.gov/articles/PMC11741407/
  56. https://pmc.ncbi.nlm.nih.gov/articles/PMC4603997/
  57. https://pmc.ncbi.nlm.nih.gov/articles/PMC5528162/
  58. https://www.frontiersin.org/journals/synaptic-neuroscience/articles/10.3389/fnsyn.2022.1002960/full
  59. https://www.sciencedirect.com/science/article/pii/S2589004222005156
  60. https://www.sciencedirect.com/science/article/pii/S2211124721013115
  61. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0057054
  62. https://nba.uth.tmc.edu/neuroscience/m/s3/chapter04.html
  63. https://www.sciencedirect.com/science/article/abs/pii/S0006899312009353
  64. https://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1004233
  65. https://pmc.ncbi.nlm.nih.gov/articles/PMC4409064/
  66. https://www.jneurosci.org/content/26/50/12921
  67. https://pmc.ncbi.nlm.nih.gov/articles/PMC6726018/
  68. https://www.jneurosci.org/content/27/7/1594
  69. https://pubmed.ncbi.nlm.nih.gov/9054347/
  70. https://pmc.ncbi.nlm.nih.gov/articles/PMC3134536/
  71. https://www.jneurosci.org/content/19/5/1876
  72. https://pmc.ncbi.nlm.nih.gov/articles/PMC2788608/
  73. https://pmc.ncbi.nlm.nih.gov/articles/PMC3124757/
  74. https://www.sciencedirect.com/science/article/pii/S0306453021004704
  75. https://pmc.ncbi.nlm.nih.gov/articles/PMC4596942/
  76. https://www.nature.com/articles/s41467-023-42777-3
  77. https://pmc.ncbi.nlm.nih.gov/articles/PMC3955116/
  78. https://pmc.ncbi.nlm.nih.gov/articles/PMC3108575/
  79. https://pmc.ncbi.nlm.nih.gov/articles/PMC4523429/
  80. https://pmc.ncbi.nlm.nih.gov/articles/PMC4293232/
  81. https://pmc.ncbi.nlm.nih.gov/articles/PMC6721865/
  82. https://pmc.ncbi.nlm.nih.gov/articles/PMC4517533/
  83. https://pmc.ncbi.nlm.nih.gov/articles/PMC3181806/
  84. https://link.springer.com/article/10.1007/s00401-010-0711-0
  85. https://pmc.ncbi.nlm.nih.gov/articles/PMC8546598/
  86. https://www.ncbi.nlm.nih.gov/books/NBK559166/
  87. https://pmc.ncbi.nlm.nih.gov/articles/PMC3337013/
  88. https://pmc.ncbi.nlm.nih.gov/articles/PMC10448058/
  89. https://pmc.ncbi.nlm.nih.gov/articles/PMC10451670/
  90. https://pmc.ncbi.nlm.nih.gov/articles/PMC4460554/
  91. https://pmc.ncbi.nlm.nih.gov/articles/PMC2517242/
  92. https://pmc.ncbi.nlm.nih.gov/articles/PMC6401206/
  93. https://www.nature.com/articles/s41398-017-0071-9
  94. https://www.sciencedirect.com/science/article/pii/S0896627310001054
  95. https://pmc.ncbi.nlm.nih.gov/articles/PMC3640293/
  96. https://pubmed.ncbi.nlm.nih.gov/22368240/
  97. https://pubmed.ncbi.nlm.nih.gov/16176432/
  98. https://pubmed.ncbi.nlm.nih.gov/26999477/
  99. https://pubmed.ncbi.nlm.nih.gov/17224135/
  100. https://pubmed.ncbi.nlm.nih.gov/26928064/
  101. https://pubmed.ncbi.nlm.nih.gov/21480545/
  102. https://pmc.ncbi.nlm.nih.gov/articles/PMC11919028/
  103. https://academic.oup.com/brain/article/144/7/1943/6168126
  104. https://www.sciencedirect.com/science/article/pii/S0149763425001289
  105. https://pmc.ncbi.nlm.nih.gov/articles/PMC1920543/
  106. https://pmc.ncbi.nlm.nih.gov/articles/PMC2948245/
  107. https://www.pnas.org/doi/10.1073/pnas.1010654108
  108. https://www.annualreviews.org/doi/pdf/10.1146/annurev-psych-122414-033457
  109. https://www.sciencedirect.com/science/article/pii/S0149763413000468
  110. https://jamanetwork.com/journals/jamaneurology/fullarticle/794743
  111. https://pmc.ncbi.nlm.nih.gov/articles/PMC58680/
  112. https://www.pnas.org/doi/pdf/10.1073/pnas.191352698
  113. https://www.sciencedirect.com/science/article/pii/S1053811916000070
  114. https://pmc.ncbi.nlm.nih.gov/articles/PMC4458066/
  115. https://pmc.ncbi.nlm.nih.gov/articles/PMC4106030/
  116. https://pmc.ncbi.nlm.nih.gov/articles/PMC9685818/
  117. https://www.ebsco.com/research-starters/history/willis-identifies-basal-ganglia
  118. https://www.sciencedirect.com/science/article/abs/pii/B9780128022061000027
  119. https://www.prd-journal.com/article/S1353-8020%2806%2900232-X/fulltext
  120. https://pubmed.ncbi.nlm.nih.gov/11983801/
  121. https://www.nobelprize.org/prizes/medicine/2000/carlsson/facts/
  122. https://pmc.ncbi.nlm.nih.gov/articles/PMC3834057/
  123. https://academic.oup.com/cercor/article/18/12/2735/362114
  124. https://pmc.ncbi.nlm.nih.gov/articles/PMC3545026/
  125. https://www.nature.com/articles/s41593-020-00777-7
  126. https://pmc.ncbi.nlm.nih.gov/articles/PMC10499063/
  127. https://www.sciencedirect.com/science/article/pii/S2211124724002444
  128. https://pmc.ncbi.nlm.nih.gov/articles/PMC2822067/
  129. https://pmc.ncbi.nlm.nih.gov/articles/PMC6523536/
  130. https://pmc.ncbi.nlm.nih.gov/articles/PMC3966536/
  131. https://www.nature.com/articles/s41598-023-29488-x
  132. https://pmc.ncbi.nlm.nih.gov/articles/PMC10440267/
  133. https://pmc.ncbi.nlm.nih.gov/articles/PMC7162658/
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