Functionally, the striatum coordinates multiple aspects ofcognition, including bothmotor and action planning,decision-making,motivation,reinforcement, andreward perception.[2][3][4] The striatum is made up of thecaudate nucleus, theputamen, and the ventral striatum.[7] The lentiform nucleus is made up of the larger putamen, and the smallerglobus 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.
Inprimates, the striatum is divided into the ventral striatum and the dorsal striatum, subdivisions that are based upon function and connections. Theventral striatum consists of thenucleus accumbens and theolfactory tubercle. Thedorsal striatum consists of thecaudate nucleus and theputamen. Awhite matternerve tract (theinternal capsule) in the dorsal striatum separates the caudate nucleus and the putamen.[4] Anatomically, the termstriatum describes its striped (striated) appearance of grey-and-white matter.[9]
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.
The dorsal striatum is composed of thecaudate nucleus and 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.[14] The dorsomedial region receives projections from the frontal and the parietal cortices. The dorsolateral region receives projections from the sensorimotor cortex.[15]
Neurochemistry studies have usedstaining techniques on 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.[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]
Medium spiny neurons (MSNs), which are the principal neurons of the striatum.[2] They areGABAergic 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 twocharacteristic types:D1-type MSNs andD2-type MSNs.[2][4][18] A subpopulation of MSNs contain both D1-type and D2-type receptors, with approximately 40% of striatal MSNs expressing bothDRD1 andDRD2mRNA.[2][4][18]
Cholinergicinterneurons 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 thesubstantia nigra.[19][20] The large aspiny cholinergic interneurons themselves are affected by dopamine throughD5 dopamine receptors.[21] Dopamine also directly controls communication between cholinergic interneurons.[22][23]
There are many types of GABAergic interneurons.[24] The best known areparvalbumin expressing interneurons, also known asfast-spiking interneurons, which participate in powerfulfeedforward inhibition of principal neurons.[25] Also, there are GABAergic interneurons that expresstyrosine hydroxylase,[26]somatostatin,nitric oxide synthase andneuropeptide-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] Theseneurons of the striatum are not distributed evenly.[24]
There are two regions ofneurogenesis in the brain – thesubventricular zone (SVZ) in thelateral ventricles, and thedentate gyrus in thehippocampal 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 anischemic 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 theolfactory bulb but this traffic is diverted to the striatum after an ischemic stroke. However, few of the new developed neurons survive.[32]
Simplified diagram of frontal cortex to striatum to thalamus pathways –frontostriatal circuitOverview 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 excitatoryglutamatergic pathways,red arrows refer to inhibitoryGABAergic pathways andturquoise arrows refer todopaminergic pathways that are excitatory on thedirect pathway and inhibitory on theindirect pathway.
The largest connection is from thecortex, in terms of cell axons. Many parts of theneocortexinnervate the dorsal striatum. The corticalpyramidal 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 thedendritic spines of the spiny neurons. They areglutamatergic, exciting striatal neurons.
Another well-known afferent is thenigrostriatal connection arising from the neurons of thesubstantia 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 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).
The main nucleus of the basal ganglia is the striatum which projects directly to the globus pallidus via a pathway ofstriatopallidal 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), thepars compacta of thesubstantia nigra (SNc), and thepars 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 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 area and another through the substantia nigra to the ventral anterior nuclei of the thalamus and from there to thefrontal cortex and the occulomotor cortex.
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 oflanguage processing, as most models only include cortical regions, integrative models are becoming more popular in light of imaging studies, lesion studies onaphasic patients, and studies of language disorders concomitant with diseases known to affect the striatum likeParkinson's andHuntington's disease.[43]
Metabotropicdopamine 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 byaversive,novel,[46]unexpected, or intensestimuli, and cues associated with such events.[47]fMRI evidence suggests that the common property linking these stimuli, to which the striatum is reacting, issalience 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 theprefrontal cortex is relevant for behavior, particularly adolescent development as proposed by thedual systems model.[51]
The mesolimbic hypothesis ofschizophrenia has long emphasized the role of hyperdopaminergia in themesolimbic pathway, which extends from theventral 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] Mostantipsychotic treatments exert their effects by reducing dopamine binding to receptors in this region.[58] More recent evidence, however, suggests that the pathway from thesubstantia 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]
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 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.[63]
Dysfunction in the ventral striatum can lead to a variety of disorders, most notablydepression andobsessive-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]
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: thecaudate nucleus and leftputamen. Lesions localized to the caudate nucleus, as well as direct electrical stimulation, can result inlexical 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]
In the seventeenth and eighteenth centuries, the termcorpus striatum was used to designate many distinct, deep, infracortical elements of the[which?] hemisphere.[69][full citation needed] Etymologically, it is derived from (Latin)striatus[70] = "grooved, striated" and the Englishstriated = having parallel lines or grooves on the surface.[71] In 1876David 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 andOskar Vogt simplified the nomenclature by proposing the termstriatum for all elements in thebasal ganglia built with striatal elements: thecaudate nucleus, theputamen, and thefundus striati,[77] which is the ventral part linking the two preceding together ventrally to the inferior part of theinternal capsule.
The termneostriatum 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, includingMedical Subject Headings.[78]
Inbirds the term used was thepaleostriatum augmentatum, while in the new avian terminology listing (as of 2002) forneostriatum this has been changed to thenidopallium.[79]
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