Basal ganglia

Basal ganglia labeled at top right.

Basal ganglia on underneath view ofbrain

Details

Part of Cerebrum

Identifiers

Latin nuclei basales

MeSH D001479

NeuroNames 224, 2677

NeuroLex ID birnlex_826

TA A14.1.09.501

FMA 84013

Anatomical terms of neuroanatomy

Basal gangliaThe basal ganglia (or basal nuclei) is a group of subcortical nuclei, of variedorigin, in the brains of vertebrates, including humans, which are situated at thebase of the forebrain. There are some differences in the basal ganglia ofprimates. Basal ganglia are strongly interconnected with the cerebral cortex,thalamus, and brainstem, as well as several other brain areas. The basal gangliaare associated with a variety of functions, including control of voluntary motormovements, procedural learning, habit learning, eye movements, cognition,[1]

and emotion.[2]

The main components of the basal ganglia – as defined functionally – are thestriatum; both dorsal striatum (caudate nucleus and putamen) and ventralstriatum (nucleus accumbens and olfactory tubercle), globus pallidus, ventralpallidum, substantia nigra, and subthalamic nucleus.[3] Each of thesecomponents has a complex internal anatomical and neurochemical organization.The largest component, the striatum (dorsal and ventral), receives input frommany brain areas beyond the basal ganglia, but only sends output to othercomponents of the basal ganglia. The pallidum receives input from the striatum,and sends inhibitory output to a number of motor-related areas. The substantianigra is the source of the striatal input of the neurotransmitter dopamine, whichplays an important role in basal ganglia function. The subthalamic nucleusreceives input mainly from the striatum and cerebral cortex, and projects to theglobus pallidus.

Popular theories implicate the basal ganglia primarily in action selection – inhelping to decide which of several possible behaviors to execute at any giventime. In more specific terms, the basal ganglia's primary function is likely tocontrol and regulate activities of the motor and premotor cortical areas so thatvoluntary movements can be performed smoothly.[1][4] Experimental studiesshow that the basal ganglia exert an inhibitory influence on a number of motorsystems, and that a release of this inhibition permits a motor system to becomeactive. The "behavior switching" that takes place within the basal ganglia isinfluenced by signals from many parts of the brain, including the prefrontalcortex, which plays a key role in executive functions.[2][5]

The basal ganglia are of major importance for normal brain function andbehaviour. Their dysfunction results in a wide range of neurological conditionsincluding disorders of behaviour control and movement. Those of behaviourinclude Tourette syndrome, obsessive–compulsive disorder, and addiction.Movement disorders include, most notably Parkinson's disease, which involvesdegeneration of the dopamine-producing cells in the substantia nigra,Huntington's disease, which primarily involves damage to thestriatum,[1][3]dystonia, and more rarely hemiballismus. The basal ganglia have alimbic sector whose components are assigned distinct names: the nucleusaccumbens, ventral pallidum, and ventral tegmental area (VTA). There is considerable evidence that this limbic part plays a centralrole in reward learning, particularly the mesolimbic pathway from the VTA to the nucleus accumbens that uses the neurotransmitter

dopamine. A number of highly addictive drugs, including cocaine, amphetamine, and nicotine, are thought to work by increasing theefficacy of this dopamine signal. There is also evidence implicating overactivity of the VTA dopaminergic projection inschizophrenia.[6]

StructureStriatumPallidumSubstantia nigraSubthalamic nucleusCircuit connectionsNeurotransmittersFunctional connectivity

FunctionEye movementsRole in motivationDecision makingWorking memory

Clinical significance

HistoryTerminology

Other animals

See also

References

External links

In terms of development, the human central nervous system is often classified based on the original three primitive vesicles fromwhich it develops: These primary vesicles form in the normal development of the neural tube of the embryo and initially include theprosencephalon, mesencephalon, and rhombencephalon, in rostral to caudal (from head to tail) orientation. Later in development ofthe nervous system each section itself turns into smaller components. During development, the cells that migrate tangentially to formthe basal ganglia are directed by the lateral and medial ganglionic eminences.[7] The following table demonstrates this developmentalclassification and traces it to the anatomic structures found in the basal ganglia.[1][3][8] The structures relevant to the basal ganglia areshown in bold.

Primary division ofthe neural tube

Secondarysubdivision Final segments in a human adult

Prosencephalon 1. Telencephalon2. Diencephalon

1. On each side of the brain: the cerebral cortices, caudate,putamen, hypothalamus

2. Globus pallidus, ventral pallidum, thalamus, subthalamus,epithalamus, subthalamic nucleus

Mesencephalon 1. Mesencephalon 1. Mesencephalon (midbrain): substantia nigra pars compacta(SNc), substantia nigra pars reticulata (SNr)

Rhombencephalon 1. Metencephalon2. Myelencephalon

1. Pons and cerebellum2. Medulla

Contents

Structure

The basal ganglia form a fundamental component of the cerebrum. In contrast to thecortical layer that lines the surface of the forebrain, the basal ganglia are a collectionof distinct masses of gray matter lying deep in the brain not far from the junction ofthe thalamus. They lie to the side of and surround the thalamus.[9] Like most parts ofthe brain, the basal ganglia consist of left and right sides that are virtual mirrorimages of each other.

In terms of anatomy, the basal ganglia are divided into four distinct structures,depending on how superior or rostral they are (in other words depending on howclose to the top of the head they are): Two of them, the striatum and the pallidum,are relatively large; the other two, the substantianigra and the subthalamic nucleus, are smaller. Inthe illustration to the right, two coronal sectionsof the human brain show the location of the basalganglia components. Of note, and not seen in thissection, the subthalamic nucleus and substantianigra lie farther back (posteriorly) in the brainthan the striatum and pallidum.

The striatum is a subcortical structure generally divided into the dorsal striatum andventral striatum, although a medial lateral classification has been suggested to bemore relevant behaviorally[10] and is being more widely used.[11]

The striatum is composed mostly of medium spiny neurons. These GABAergicneurons project to the external (lateral) globus pallidus and internal (medial) globuspallidus as well as the substantia nigra pars reticulata. The projections into theglobus pallidus and substantia nigra are primarily dopaminergic, although

enkephalin, dynorphin and substance P are expressed. The striatum also contains interneurons that are classified into nitrergicneurons (due to use of nitric oxide as a neurotransmitter), tonically active cholinergic interneurons, parvalbumin-expressing neuronsand calretinin-expressing neurons.[12] The dorsal striatum receives significant glutamatergic inputs from the cortex, as well asdopaminergic inputs from the substantia nigra pars compacta. The dorsal striatum is generally considered to be involved insensorimotor activities. The ventral striatum receives glutamatergic inputs from the limbic areas as well as dopaminergic inputs fromthe VTA, via the mesolimbic pathway. The ventral striatum is believed to play a role in reward and other limbic functions.[13] Thedorsal striatum is divided into the caudate and putamen by the internal capsule while the ventral striatum is composed of the nucleusaccumbens and olfactory tubercle.[14][15] The caudate has three primary regions of connectivity, with the head of the caudatedemonstrating connectivity to the prefrontal cortex, cingulate cortex and amygdala. The body and tail show differentiation betweenthe dorsolateral rim and ventral caudate, projecting to the sensorimotor and limbic regions of the striatum respectively.[16]

Striatopallidal fibres connect the striatum to the pallidus.

The pallidum consists of a large structure called the globus pallidus ("pale globe") together with a smaller ventral extension called theventral pallidum. The globus pallidus appears as a single neural mass, but can be divided into two functionally distinct parts, calledthe internal (or medial) and external (lateral) segments, abbreviated GPi and GPe.[1] Both segments contain primarily GABAergicneurons, which therefore have inhibitory effects on their targets. The two segments participate in distinct neural circuits. The GPe,

Video of relevant anatomyPlay media

Coronal slices of human brain showing the basal ganglia. Whitematter is shown in dark gray, gray matter is shown in light gray. Anterior: striatum, globus pallidus (GPe and GPi) Posterior: subthalamic nucleus (STN), substantia nigra (SN)

Striatum

Basal ganglia

Pallidum

receives input mainly from the striatum, and projects to the subthalamic nucleus. The GPi, receives signals from the striatum via the"direct" and "indirect" pathways. Pallidal neurons operate using a disinhibition principle. These neurons fire at steady high rates inthe absence of input, and signals from the striatum cause them to pause or reduce their rate of firing. Because pallidal neuronsthemselves have inhibitory effects on their targets, the net effect of striatal input to the pallidum is a reduction of the tonic inhibitionexerted by pallidal cells on their targets (disinhibition) with an increased rate of firing in the targets.

The substantia nigra is a midbrain gray matter portion of the basal ganglia that hastwo parts – the pars compacta (SNc) and the pars reticulata (SNr). SNr often worksin unison with GPi, and the SNr-GPi complex inhibits the thalamus. Substantia nigrapars compacta (SNc) however, produces the neurotransmitter dopamine, which isvery significant in maintaining balance in the striatal pathway. The circuit portionbelow explains the role and circuit connections of each of the components of thebasal ganglia.

The subthalamic nucleus is a diencephalic gray matter portion of the basal ganglia, and the only portion of the ganglia that producesan excitatory neurotransmitter, glutamate. The role of the subthalamic nucleus is to stimulate the SNr-GPi complex and it is part ofthe indirect pathway. The subthalamic nucleus receives inhibitory input from the external part of the globus pallidus and sendsexcitatory input to the GPi.

Multiple models of basal ganglia circuits and function have been proposed, howeverthere have been questions raised about the strict divisions of the direct and indirectpathways, their possible overlap and regulation.[17] The circuitry models has evolvedsince the first proposed model in the 1990s by DeLong in the parallel processing model,in which the cortex and substantia nigra pars compacta project into the dorsal striatumgiving rise to an inhibitory indirect and excitatory direct pathway.

The inhibitory indirect pathway involved the inhibition of the globus pallidusexternus, allowing for the disinhibition of the globus pallidus internus(through STN) allowing it to inhibit the thalamus.The direct or excitatory pathway involved the disinhibition of the thalamusthrough the inhibition of the GPi/SNr. However the speed of the directpathway would not be concordant with the indirect pathway in this modelleading to problems with it. To get over this, a hyperdirect pathway wherethe cortex sends glutamatergic projections through the subthalamic nucleusexciting the inhibitory GPe under the center surround model, as well as ashorter indirect pathway have been proposed.

Generally, the basal ganglia circuitry is divided into a limbic, twoassociative(prefrontal), an oculomotor and one motor pathway. The motor andoculomotor are sometimes grouped into one motor pathway. The 5 general pathways areorganized as follows:[18]

The motor loop involving projections from the supplementary motor area,arcuate premotor area, motor cortex and somatosensory cortex into theputamen, which projects into the ventrolateral GPi and caudolateral SNrwhich projects into the cortex through the ventralis lateralis pars medialisand ventralis lateralis pars orialis.The oculomotor loop involved projections from the frontal eye fields, thedorsolateral prefrontal cortex (DLPFC), and the posterior parietal cortex into the caudate, into the caudal

dorsomedial GPi and

Substantia nigra

Location of the substantia nigrawithin the basal ganglia

Subthalamic nucleus

Circuit connections

Connectivity diagram showingexcitatory glutamatergic pathwaysas red, inhibitory GABAergicpathways as blue, andmodulatory dopaminergicpathways as magenta.(Abbreviations: GPe: globuspallidus external; GPi: globuspallidus internal; STN:subthalamic nucleus; SNc:substantia nigra pars compacta;SNr: substantia nigra parsreticulata)

dorsomedial GPi andventrolateral SNr, finallylooping back into thecortex through the lateralventralis anterior parsmagnocellularis(VAmc).The firstcognitive/associativepathway proposes apathway from theDLPFC, into thedorsolateral caudate,followed by a projectioninto the lateraldosomedial GPi, androstral SNr beforeprojecting into the lateralVAmc and medial parsmagnocellularis.The secondcognitive/associativepathway proposed is acircuit projecting from thelateral orbitofrontalcortex, the temporalgyrus, and anteriorcingulate cortex into theventromedial caudate,

followed by a projection into the lateromedial GPi, and rostrolateral SNr before looping into the cortex via the medialVAmc and medial magnocellularis.The limbic circuit involving the projections from the ACC, hippocampus, entorhinal cortex, and insula into the ventralstriatum, then into the rostrodorsal GPi, ventral palladium and rostrodorsal SNr, followed by a loop back into thecortex through the posteromedial part of the medial dorsal nucleus.[19] However, more subdivisions of loops havebeen proposed, up to 20,000.[20]

The direct pathway, originating in the dorsal striatum inhibits the GPi and SNr, resulting in a net disinhibition or excitation of thethalamus. This pathway consist of medium spiny neurons (MSNs) that express dopamine receptor D1, muscarinic acetylcholinereceptor M4, and adenosine receptor A1.[21] The direct pathway has been proposed to facilitate motor actions, timing of motoractions, gating of working memory, and motor responses to specific stimuli.[20]

The (long) indirect pathway originates in the dorsal striatum and inhibits the GPe, resulting in disinhibition of the GPi which is thenfree to inhibit the thalamus. This pathway consists of MSNs that express dopamine receptor D2, muscarinic acetylcholine receptorM1, and adenosine receptor A2a.[21] This pathway has been proposed to result in global motor inhibition(inhibition of all motoractivity), and termination of responses. Another shorter indirect pathway has been proposed, which involves cortical excitation of thesubthalamic nucleus resulting in direct excitation of the GPe, and inhibition of the thalamus. This pathway is proposed to result ininhibition of specific motor programs based on associative learning.[20]

A combination of these indirect pathways resulting in a hyperdirect pathway that results in inhibition of basal ganglia inputs besidesone specific focus has been proposed as part of the center surround theory.[22][23] This hyperdirect pathway is proposed to inhibitpremature responses, or globally inhibit the basal ganglia to allow for more specific top down control by the cortex.[20]

The interactions of these pathways are currently under debate. Some say that all pathways directly antagonize each other in a "pushpull" fashion, while others support the center surround theory, in which one focused input into the cortex is protected by inhibition ofcompeting inputs by the rest of the indirect pathways.[20]

The basal ganglia contains many afferent glutamatergic inputs, with predominantly GABAergic efferent fibers, modulatorycholinergic pathways, significant dopamine in the pathways originating in the ventral tegmental area and substantia nigra, as well asvarious neuropeptides. Neuropeptides found in the basal ganglia include substance P, neurokinin A, cholecystokinin, neurotensin,

Connectivity of the basal ganglia asrevealed by diffusion spectrumimaging based on thirty subjects fromthe Human Connectome Project.Direct, indirect and hyperdirectpathways are visualized in differentcolors (see legend). Subcorticalstructures are rendered based on theHarvard-Oxford subcortical thalamusas well as the Basal Ganglia atlas(other structures). Rendering wasgenerated using TrackVis software.

The left side of Fig.1 shows a region of theprefrontal cortex receiving multiple inputsfrom other regions, as cortico-corticalactivity. The input from B is the strongest ofthese. The right side of Fig. 1 shows theinput signals also being fed to the basalganglia circuitry. The output from here, backto the same region, is shown to modify thestrength of the input from B, by addingstrength to the input from C therebymodifying the strongest signal from B to C.(Thalamic involvement is implicit but notshown).

Neurotransmitters

neurokinin B, neuropeptide Y, somatostatin, dynorphin, enkephaline. Otherneuromodulators found in the basal ganglia include nitric oxide, carbon monoxide,and phenylethylamine.[24]

The functional connectivity, measured by regional co-activation during functionalneuroimaging studies, is broadly consistent with the parallel processing models ofbasal ganglia function. The putamen was generally coactivated with motor areassuch as the supplementary motor area, caudal anterior cingulate cortex and primarymotor cortex, while the caudate and rostral putamen were more frequentlycoactivated with the rostral ACC and DLPFC. The ventral striatum was significantlyassociated with the amygdala and hippocampus, which although was not included inthe first formulations of basal ganglia models, has been an addition to more recentmodels.[25]

One intensively studied function of the basal ganglia is its role in controlling eyemovements.[26] Eye movement is influenced by an extensive network of brainregions that converges on a midbrain area called the superior colliculus (SC). TheSC is a layered structure whose layers form two-dimensional retinotopic maps ofvisual space. A "bump" of neural activity in the deep layers of the SC drives an eyemovement directed toward the corresponding point in space.

The SC receives a strong inhibitory projection from the basal ganglia, originating in the substantia nigra pars reticulata (SNr).[26]

Neurons in the SNr usually fire continuously at high rates, but at the onset of an eye movement they "pause", thereby releasing theSC from inhibition. Eye movements of all types are associated with "pausing" in the SNr; however, individual SNr neurons may bemore strongly associated with some types of movements than others. Neurons in some parts of the caudate nucleus also show activityrelated to eye movements. Since the great majority of caudate cells fire at very low rates, this activity almost always shows up as anincrease in firing rate. Thus, eye movements begin with activation in the caudate nucleus, which inhibits the SNr via the directGABAergic projections, which in turn disinhibits the SC.

Extracellular dopamine in the basal ganglia has been linked to motivational states in rodents, with high levels being linked to satiated"euphoria", medium levels with seeking, and low with aversion. The limbic basal ganglia circuits are influenced heavily byextracellular dopamine. Increased dopamine results in inhibition of the Ventral pallidum, entopeduncular nucleus, and substantianigra pars reticulata, resulting in disinhibition of the thalamus. This model of direct D1, and indirect D2 pathways explain whyselective agonists of each receptor are not rewarding, as activity at both pathways is required for disinhibition. The disinhibition ofthe thalamus leads to activation of the prefrontal cortex and ventral striatum, selective for increased D1 activity leading to reward.[19]

Two models have been proposed for the basal ganglia, one being that actions are generated by a "critic" in the ventral striatum andestimates value, and the actions are carried out by an "actor" in the dorsal striatum. Another model proposes the basal ganglia acts asa selection mechanism, where actions are generated in the cortex and are selected based on context by the basal ganglia.[27] The

Diagram shows two coronal slicesthat have been superimposed toinclude the involved basal gangliastructures. Green arrows (+) refer toexcitatory glutamatergic pathways,red arrows (–) refer to inhibitoryGABAergic pathways and turquoisearrows refer to dopaminergicpathways that are excitatory on thedirect pathway and inhibitory on theindirect pathway.

Functional connectivity

Function

Eye movements

Role in motivation

Decision making

CBGTC loop is also involved in reward discounting, with firing increasing with an unexpected or greater than expected reward.[28]

One review supported the idea that the cortex was involved in learning actions regardless of their outcome, while the basal gangliawas involved in selecting appropriate actions based on associative reward based trial and error learning.[29]

The basal ganglia has been proposed to gate what enters and what doesn't enter working memory. One hypothesis proposes that thedirect pathway (Go, or excitatory) allows information into the PFC, where it stays independent of the pathway, however anothertheory proposes that in order for information to stay in the PFC the direct pathway needs to continue reverberating. The short indirectpathway has been proposed to, in a direct push pull antagonism with the direct pathway, close the gate to the PFC. Together thesemechanisms regulate working memory focus.[20]

Basal ganglia disease is a group of movement disorders that result from either excessive output from the basal ganglia to the thalamus– hypokinetic disorders, or from insufficient output – hyperkinetic disorders. Hypokinetic disorders arise from an excessive outputfrom the basal ganglia, which inhibits the output from the thalamus to the cortex, and thus limits voluntary movement. Hyperkineticdisorders result from a low output from the basal ganglia to the thalamus which gives not enough inhibition to the thalamicprojections to the cortex and thus gives uncontrolled/involuntary movements. Dysfunction of the basal ganglia circuitry can also leadto other disorders.[30]

The following is a list of disorders that have been linked to the basal ganglia:

AddictionAthetosisAthymhormic syndrome (PAP syndrome)Attention-deficit hyperactivity disorder (ADHD)BlepharospasmBruxismCerebral palsy: basal ganglia damage during second and third trimester of pregnancyChoreaDystoniaFahr's diseaseForeign accent syndrome (FAS)Huntington's diseaseKernicterusLesch–Nyhan syndrome

Major Depressive Disorder [31]

Obsessive-compulsive disorder[32][33]

Other anxiety disorders [33]

PANDASParkinson's diseaseSpasmodic dysphonia

Stuttering[34]

Sydenham's choreaTardive dyskinesia, caused by chronic antipsychotic treatmentTourette's disorderWilson's disease

Working memory

Clinical significance

History

The acceptance that the basal ganglia system constitutes one major cerebral system took time to arise. The first anatomicalidentification of distinct subcortical structures was published by Thomas Willis in 1664.[35] For many years, the term corpusstriatum[36] was used to describe a large group of subcortical elements, some of which were later discovered to be functionallyunrelated.[37] For many years, the putamen and the caudate nucleus were not associated with each other. Instead, the putamen wasassociated with the pallidum in what was called the nucleus lenticularis or nucleus lentiformis.

A thorough reconsideration by Cécile and Oskar Vogt (1941) simplified the description of the basal ganglia by proposing the termstriatum to describe the group of structures consisting of the caudate nucleus, the putamen, and the mass linking them ventrally, thenucleus accumbens. The striatum was named on the basis of the striated (striped) appearance created by radiating dense bundles ofstriato-pallido-nigral axons, described by anatomist Samuel Alexander Kinnier Wilson (1912) as "pencil-like".

The anatomical link of the striatum with its primary targets, the pallidum and the substantia nigra, was discovered later. The nameglobus pallidus was attributed by Déjerine to Burdach (1822). For this, the Vogts proposed the simpler "pallidum". The term "locusniger" was introduced by Félix Vicq-d'Azyr as tache noire in (1786), though that structure has since become known as the substantianigra, due to contributions by Von Sömmering in 1788. The structural similarity between the substantia nigra and globus pallidus wasnoted by Mirto in 1896. Together, the two are known as the pallidonigral ensemble, which represents the core of the basal ganglia.Altogether, the main structures of the basal ganglia are linked to each other by the striato-pallido-nigral bundle, which passes throughthe pallidum, crosses the internal capsule as the "comb bundle of Edinger", and finally reaches the substantia nigra.

Additional structures that later became associated with the basal ganglia are the "body of Luys" (1865) (nucleus of Luys on thefigure) or subthalamic nucleus, whose lesion was known to produce movement disorders. More recently, other areas such as thecentromedian nucleus and the pedunculopontine complex have been thought to be regulators of the basal ganglia.

Near the beginning of the 20th century, the basal ganglia system was first associated with motor functions, as lesions of these areaswould often result in disordered movement in humans (chorea, athetosis, Parkinson's disease).

The nomenclature of the basal ganglia system and its components has always been problematic. Early anatomists, seeing themacroscopic anatomical structure but knowing nothing of the cellular architecture or neurochemistry, grouped together componentsthat are now believed to have distinct functions (such as the internal and external segments of the globus pallidus), and gave distinctnames to components that are now thought to be functionally parts of a single structure (such as the caudate nucleus and putamen).

The term "basal" comes from the fact that most of its elements are located in the basal part of the forebrain. The term ganglia is amisnomer: In modern usage, neural clusters are called "ganglia" only in the peripheral nervous system; in the central nervous systemthey are called "nuclei". For this reason, the basal ganglia are also occasionally known as the "basal nuclei".[38] Terminologiaanatomica (1998), the international authority for anatomical naming, retained "nuclei basales", but this is not commonly used.

The International Basal Ganglia Society (IBAGS)[39] informally considers the basal ganglia to be made up of the striatum, thepallidum (with two nuclei), the substantia nigra (with its two distinct parts), and the subthalamic nucleus, whereas Terminologiaanatomica excludes the last two. Some neurologists have included the centromedian nucleus of the thalamus as part of the basalganglia,[40][41] and some have also included the pedunculopontine nucleus.[42]

The basal ganglia form one of the basic components of the forebrain, and can be recognized in all species of vertebrates.[43] Even inthe lamprey (generally considered one of the most primitive of vertebrates), striatal, pallidal, and nigral elements can be identified onthe basis of anatomy and histochemistry.[44]

The names given to the various nuclei of the basal ganglia are different in different species. In cats and rodents the internal globuspallidus is known as the entopeduncular nucleus.[45] In birds the striatum is called the paleostriatum augmentatum and the externalglobus pallidus is called the paleostriatum primitivum.

Terminology

Other animals

A clear emergent issue in comparative anatomy of the basal ganglia is the development of this system through phylogeny as aconvergent cortically re-entrant loop in conjunction with the development and expansion of the cortical mantle. There is controversy,however, regarding the extent to which convergent selective processing occurs versus segregated parallel processing within re-entrantclosed loops of the basal ganglia. Regardless, the transformation of the basal ganglia into a cortically re-entrant system in mammalianevolution occurs through a re-direction of pallidal (or "paleostriatum primitivum") output from midbrain targets such as the superiorcolliculus, as occurs in sauropsid brain, to specific regions of the ventral thalamus and from there back to specified regions of thecerebral cortex that form a subset of those cortical regions projecting into the striatum. The abrupt rostral re-direction of the pathwayfrom the internal segment of the globus pallidus into the ventral thalamus—via the path of the ansa lenticularis—could be viewed asa footprint of this evolutionary transformation of basal ganglia outflow and targeted influence.

Alexander CoolsNathaniel A. Buchwald

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See also

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