Wikipedia

Striatum

"Neostriatum" redirects here. For the avian brain region formerly called the neostriatum, seenidopallium.

Thestriatum(pl.:striata) orcorpus striatum[5]is a cluster of interconnectednucleithat make up the largest structure of the subcorticalbasal ganglia.[6]The striatum is a critical component of themotorandreward systems;receivesglutamatergicanddopaminergicinputs from different sources; and serves as the primary input to the rest of the basal ganglia.

Striatum
Striatum shown in green with otherbasal gangliaandthalamus.Small region in yellow is theamygdala
Tractographyshowing 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
NeuroLexIDbirnlex_1672
TA98A14.1.09.516
A14.1.09.515
TA25559
FMA77616 77618, 77616
Anatomical terms of neuroanatomy

Functionally, the striatum coordinates multiple aspects ofcognition,including bothmotor and action planning,decision-making,motivation,reinforcement,andrewardperception.[2][3][4]The striatum is made up of thecaudate nucleusand thelentiform nucleus.[7][8]However, some authors believe it is made up ofcaudate nucleus,putamen,and ventral striatum.[9]The lentiform nucleus is made up of the largerputamen,and the smallerglobus pallidus.[10]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.

Inprimates,the striatum is divided into the ventral striatum and the dorsal striatum, subdivisions that are based upon function and connections. Theventralstriatum consists of thenucleus accumbensand theolfactory tubercle.Thedorsalstriatum consists of thecaudate nucleusand theputamen.Awhite matternerve tract(theinternal capsule) in the dorsal striatum separates thecaudate nucleusand theputamen.[4]Anatomically, the termstriatumdescribes its striped (striated) appearance of grey-and-white matter.[11]

Structure

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The striatum in red as seen onMRI.The striatum includes thecaudate nucleus(top), and thelentiform nucleus(theputamen(right) and theglobus pallidus(lower left))

The striatum is the largest structure of thebasal 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 thenucleus accumbensand theolfactory tubercle.[4][12]The nucleus accumbens is made up of thenucleus accumbens coreand thenucleus accumbens shell,which differ by neural populations. The olfactory tubercle receives input from theolfactory bulbbut has not been shown to play a role inprocessing smell.[12]In non-primate species, theislands of Callejaare included.[13]The ventral striatum is associated with thelimbic systemand has been implicated as a vital part of thecircuitryfor decision making and reward-related behavior.[14][15]

Dorsal striatum

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The dorsal striatum is composed of thecaudate nucleusand theputamen. Primarily it mediates cognition and involves motor and executive function. The dorsal striatum can be further subdivided into thedorsomedial striatum,and thedorsolateral striatum.Both of these areas have different roles in the acquisition of learnt behaviour and skill formation.[16]The dorsomedial region receives projections from the frontal and the parietal cortices. The dorsolateral region receives projections from the sensorimotor cortex.[17]

Matrix and striosomes

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Neurochemistrystudies have usedstaining techniqueson the striatum that have identified two distinct striatal compartments, the matrix, and thestriosome(or patch). The matrix is seen to be rich inacetylcholinesterase,while the embedded striosomes are acetylcholinesterase-poor.[18]The matrix forms the bulk of the striatum, and receives input from most areas of the cerebral cortex.[19]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.[19]

The striosomes receive input from the prefrontal cortex and give outputs to the substantia nigra pars compacta.[19]There are more striosomes present in the dorsal striatum making up 10-15% of the striatal volume, than in the ventral striatum.[18]

Cell types

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Dendritic spinesonmedium spiny neuronof striatum

Types of cells in the striatum include:

  • Medium spiny neurons(MSNs), which are the principal neurons of the striatum.[2]They areGABAergicand, 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 twocharacteristic types:D1-typeMSNs andD2-typeMSNs.[2][4][20]A subpopulation of MSNs contain both D1-type and D2-type receptors, with approximately 40% of striatal MSNs expressing bothDRD1andDRD2mRNA.[2][4][20]
  • Cholinergicinterneuronsrelease 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 thesubstantia nigra.[21][22]The large aspiny cholinergic interneurons themselves are affected by dopamine throughD5 dopamine receptors.[23]Dopamine also directly controls communication between cholinergic interneurons.[24][25]
  • There are many types of GABAergic interneurons.[26]The best known areparvalbuminexpressing interneurons, also known asfast-spikinginterneurons, which participate in powerfulfeedforwardinhibition of principal neurons.[27]Also, there are GABAergic interneurons that expresstyrosine hydroxylase,[28]somatostatin,nitric oxide synthaseandneuropeptide-y.Recently, two types of neuropeptide-y expressing GABAergic interneurons have been described in detail,[29]one of which translates synchronous activity of cholinergic interneurons into inhibition of principal neurons.[30]Theseneuronsof the striatum are not distributed evenly.[26]

There are two regions ofneurogenesisin the brain – thesubventricular zone(SVZ) in thelateral ventricles,and thedentate gyrusin thehippocampal formation.Neuroblaststhat form in the lateral ventricle adjacent to the striatum, integrate in the striatum.[31][32]This has been noted in the human striatum following anischemic stroke.Injury caused to the striatum stimulates the migration of neuroblasts from the SVZ, to the striatum, where they differentiate into adult neurons.[33]The normal passage of SVZ neuroblasts is to theolfactory bulbbut this traffic is diverted to the striatum after an ischemic stroke. However, few of the new developed neurons survive.[34]

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 arrowsrefer to excitatoryglutamatergicpathways,red arrowsrefer to inhibitoryGABAergicpathways andturquoise arrowsrefer todopaminergicpathways that are excitatory on thedirect pathwayand inhibitory on theindirect pathway.

The largest connection is from thecortex,in terms of cell axons. Many parts of theneocortexinnervatethe dorsal striatum. The corticalpyramidal neuronsprojecting to the striatum are located in layers II-VI, with the most dense projections come from layer V.[35]They end mainly on thedendritic spinesof the spiny neurons. They areglutamatergic,exciting striatal neurons.

The striatum is seen as having its own internal microcircuitry.[36]The ventral striatum receives direct input from multiple regions in thecerebral cortexand limbic structures such as theamygdala,thalamus,andhippocampus,as well as theentorhinal cortexand theinferior temporal gyrus.[37]Its primary input is to thebasal gangliasystem. Additionally, themesolimbic pathwayprojects from theventral tegmental areato thenucleus accumbensof the ventral striatum.[38]

Another well-known afferent is thenigrostriatalconnection arising from the neurons of thesubstantia nigrapars 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 thethalamus(seeprimate 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 thesubthalamic nucleus(glutamatergic) or theexternal globus pallidus(GABAergic).

Targets

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Further information:Medium spiny neuron

The primary outputs of the ventral striatum project to theventral pallidum,then themedial dorsal nucleusof thethalamus,which is part of thefrontostriatal circuit.Additionally, the ventral striatum projects to theglobus pallidus,and substantia nigra pars reticulata. Some of its other outputs include projections to theextended amygdala,lateral hypothalamus,andpedunculopontine nucleus.[39]

Striatal outputs from both the dorsal and ventral components are primarily composed ofmedium spiny neurons(MSNs), a type ofprojection neuron,which have two primaryphenotypes:"indirect" MSNs that expressD2-like receptorsand "direct" MSNs that expressD1-like receptors.[2][4]

The main nucleus of the basal ganglia is the striatum which projects directly to the globus pallidus via a pathway ofstriatopallidal fibers.[40]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), thepars compactaof thesubstantia nigra(SNc), and thepars reticulataof 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 thesuperior 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 corticalsupplementary motor areaand another through the substantia nigra to the ventral anterior nuclei of the thalamus and from there to thefrontal cortexand the occulomotor cortex.

Blood supply

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Deep penetratingstriate arteriessupply blood to the striatum. These arteries include therecurrent artery of Heubnerarising from theanterior cerebral artery,and thelenticulostriate arteriesarising from themiddle cerebral artery.[41]

Function

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The ventral striatum, and thenucleus accumbensin particular, primarily mediatesreward,cognition,reinforcement,andmotivational salience.By contrast, the dorsal striatum primarily mediates cognition involvingmotor function,certainexecutive functions(e.g.,inhibitory controlandimpulsivity), andstimulus-response learning.[2][3][4][42][43]There is a small degree of overlap, as the dorsal striatum is also a component of thereward systemthat, along with thenucleus accumbens core,mediates the encoding of new motor programs associated with future reward acquisition (e.g., theconditioned motor responseto a reward cue).[3][42]

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.[44]While the striatum is often not included in models oflanguage processing,as most models only include cortical regions, integrative models are becoming more popular in light of imaging studies, lesion studies onaphasicpatients, and studies of language disorders concomitant with diseases known to affect the striatum likeParkinson'sandHuntington'sdisease.[45]

Metabotropicdopamine receptorsare present both on spiny neurons and on cortical axon terminals.Second messengercascades triggered by activation of these dopamine receptors can modulate pre- and postsynaptic function, both in the short term and in the long term.[46][47]In humans, the striatum is activated by stimuli associated with reward, but also byaversive,novel,[48]unexpected,or intensestimuli,and cues associated with such events.[49]fMRIevidence suggests that the common property linking these stimuli, to which the striatum is reacting, issalienceunder the conditions of presentation.[50][51]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.[52]

The interplay between the striatum and theprefrontal cortexis relevant for behavior, particularly adolescent development as proposed by thedual systems model.[53]

Clinical significance

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Parkinson's disease and other movement disorders

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Parkinson's diseaseresults in loss of dopaminergic innervation to the dorsal striatum (and other basal ganglia) and a cascade of consequences.Atrophyof the striatum is also involved inHuntington's disease,andmovement disorderssuch aschorea,choreoathetosis,anddyskinesias.[54]These have also been described ascircuit disordersof the basal ganglia.[55]

Addiction

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Overview of reward structures and associated pathways

Addiction,a disorder of the brain'sreward system,arises through theoverexpressionofDeltaFosB(ΔFosB), atranscription factor,in theD1-typemedium spiny neuronsof theventral striatum.ΔFosB is aninducible genewhich is increasingly expressed in thenucleus accumbensas a result of repeatedly using an addictive drug or overexposure to other addictive stimuli.[56][57]

Bipolar disorder

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An association has been observed between striatal expression of variants of thePDE10Agene and somebipolar I disorderpatients. Variants of other genes,DISC1andGNAS,have been associated withbipolar II disorder.[58]

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 pre-frontal cortex as well as the striatal circuits.[59]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 theeukaryotic 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.[60]

Dysfunction

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Dysfunction in the ventral striatum can lead to a variety of disorders, most notablydepressionandobsessive-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.[61]

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.[62]Two subregions of the striatum have been shown to be particularly important in language: thecaudate nucleusand leftputamen.Lesions localized to the caudate nucleus, as well as direct electrical stimulation, can result inlexical paraphasiasand 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).[63]Stimulation of the putamen results in the inhibition of articulatory sequences and the inability to initiate motor speech commands.[64][65]

History

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In the seventeenth and eighteenth centuries, the termcorpus striatumwas used to designate many distinct, deep, infracortical elements of the[which?]hemisphere.[66]Etymologically, it is derived from (Latin)striatus[67]= "grooved, striated" and the Englishstriated= having parallel lines or grooves on the surface.[68]In 1876David Ferriercontributed decades of research to the subject; concluding that the corpus striatum was vital in the "organization and generation of voluntary movement".[69][70][71][72][73]In 1941,CécileandOskar Vogtsimplified the nomenclature by proposing the termstriatumfor all elements in thebasal gangliabuilt with striatal elements: thecaudate nucleus,theputamen,and thefundus striati,[74]which is the ventral part linking the two preceding together ventrally to the inferior part of theinternal capsule.

The termneostriatumwas 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, includingMedical Subject Headings.[75]

Other animals

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Inbirdsthe term used was thepaleostriatum augmentatum,and in the new avian terminology listing (as of 2002) forneostriatumthis has been changed to thenidopallium.[76]

In non-primate species, theislands of Callejaare included in the ventral striatum.[13]

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

References

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    Functional neuroimaging in humans demonstrates activation of the prefrontal cortex and caudate nucleus (part of the striatum) in tasks that demand inhibitory control of behavior....
    The brain reward circuitry that is targeted by addictive drugs normally mediates the pleasure and strengthening of behaviors associated with natural reinforcers, such as food, water, and sexual contact. Dopamine neurons in the VTA are activated by food and water, and dopamine release in the NAc is stimulated by the presence of natural reinforcers, such as food, water, or a sexual partner....
    The NAc and VTA are central components of the circuitry underlying reward and memory of reward. As previously mentioned, the activity of dopaminergic neurons in the VTA appears to be linked to reward prediction. The NAc is involved in learning associated with reinforcement and the modulation of motoric responses to stimuli that satisfy internal homeostatic needs. The shell of the NAc appears to be particularly important to initial drug actions within reward circuitry; addictive drugs appear to have a greater effect on dopamine release in the shell than in the core of the NAc.
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