Striatum

From Wikipedia, the free encyclopedia
Jump to: navigation, search
Brain: Striatum
BrainCaudatePutamen.svg
purple=caudate and putamen, orange=thalamus
Gray741.png
Two views of a model of the striatum. A: lateral aspect, B: medial aspect. (The lenticular nucleus is an alternative name for the putamen and globus pallidus.)
Latin Corpus striatum, neostriatum
NeuroNames hier-207

The striatum, also known as the neostriatum or striate nucleus, is a subcortical (i.e., inside, rather than on the outside) part of the forebrain. It receives input from the cerebral cortex and is the primary input to the basal ganglia system. In primates (including humans), the striatum is divided by a white matter tract called the internal capsule into two sectors called the caudate nucleus and putamen. The term corpus striatum occasionally refers to the striatum combined with the globus pallidus, a structure closely related to the putamen, and the lenticular nucleus refers to the putamen together with the globus pallidus.[1]

Functionally, the striatum helps coordinate motivation with body movement. It facilitates and balances motivation with both higher-level and lower-level functions, such as inhibiting one's behavior in a complex social interaction and fine-motor functions of inhibiting small voluntary movement.[2]

Structure[edit]

Cell types[edit]

The striatum is heterogeneous in terms of its component neurons.[3]

  • Spiny projection neurons, commonly referred to as medium spiny neurons, are the principal neurons of the striatum. They are GABAergic and, thus, are classified as inhibitory neurons. Depending on the species, spiny projection neurons comprise 90–95% of the total neuronal population.
  • Cholinergic interneurons release acetylcholine, which has a variety of important effects in the striatum. In humans, non-human 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.[4][5]
  • There are many types of GABAergic interneurons.[3] The best known are parvalbumin expressing interneurons, also known as fast-spiking interneurons, which participate in powerful feed-forward inhibition of principal neurons.[6] Also, there are GABAergic interneurons that express tyrosine hydroxylase,[7] somatostatin, nitric oxide synthase and neuropeptide-Y. Recently, two types of neuropeptide-y expressing GABAergic interneurons have been described in detail,[8] one of which translates synchronous activity of cholinergic interneurons into inhibition of principal neurons.[9]

Adult humans continuously produce new neurons in the striatum, and these neurons could play a possible role in new treatments for neurodegenerative disorders.[10]

Anatomical subdivisions[edit]

This is a transverse section of the striatum from a structural MR image. The striatum includes the caudate nucleus and putamen. The image also includes the globus pallidus, which is sometimes included when using the term corpus striatum.
This is a transverse section of the striatum from a structural MR image. The striatum includes the caudate nucleus (red, top) and putamen (red, right). The image also includes the globus pallidus (red, lower-left), which is sometimes included when using the term corpus striatum.

The observable anatomical subdivisions of the dorsal striatum (caudate nucleus and putamen), in essence induced by the internal capsule, do not completely overlap with now-accepted anatomo-functional subdivisions. The selective distribution of the axonal terminal arborisations of cortical sources differentiate the sensorimotor striatum, mainly putaminal but located in its dorsal part and in the lateroinferior part of the caudate. A great part of the remaining of the volume (in essence, caudate) receiving from axonal endings from the frontal, parietal, temporal cortex forms the associative striatum. The separation between these two territories is rather clearcut and observable using calbindin immunochemistry. A third entity, the most inferomedial, raises more problems, as there is no general agreement about its border with the associative striatum.

The striatum can also be differentiated based on immunochemical characteristics—in particular with regard to acetylcholinesterase—into "compartments", consisting of 'striosomes' and 'matrisomes'.

Overview of the main circuits of the basal ganglia. 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.

Inputs (afferent connections)[edit]

The most important afferent in terms of quantity of axons is the corticostriatal connection. Many parts of the neocortex innervate the dorsal striatum. The cortical pyramidal neurons projecting to the striatum are located in layers II-VI, but the most dense projections come from layer V.[11] They end mainly on the spines of the spiny neurons. They are glutamatergic, exciting striatal neurons. 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 (efferent connections)[edit]

The basal ganglia core is made up of the striatum along with the regions to which it projects directly, via the striato-pallidonigral bundle. The striato-pallidonigral bundle is a very dense bundle of sparsely myelinated axons, giving a whitish appearance. 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 (SMA) 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.

Function[edit]

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.[citation needed] The striatum is best known for its role in the planning and modulation of movement pathways but is also potentially involved in a variety of other cognitive processes involving executive function, such as working memory.[12] In humans, the striatum is activated by stimuli associated with reward, but also by aversive, novel, unexpected, or intense stimuli, and cues associated with such events.[citation needed] Recent fMRI evidence[13] suggests that the common property linking these stimuli, to which the striatum is reacting, is saliency under the conditions of presentation. A number of other brain areas and circuits are also related to reward, such as frontal areas. Further Research at the Wellcome Trust Centre for Neuroimaging at UCL (University College London) shows it to be associated with novelty-related decision-making behaviors.

For sources regarding saliency of the reward pathway (thought to be related to dopamine), one can look to the work of Dr. John D. Salamone (early to late 1990s) and Wolfram Schultz.[14] The ventral tegmental dopaminergic neurons that innervate portions of the striatum have long been accepted to be the site of rewarding feeling. Intracranial stimulation studies from the 1960s show that implants in this brain area will elicit bar pressing from rats for many hours at a time. As rewarding sensations are difficult to assess in animals, hundreds of studies over more than 30 years have shown that interference with dopamine neurotransmission impairs behavioral reward processes and their underlying neuronal mechanisms.[citation needed]

Clinical significance[edit]

Parkinson's disease[edit]

Parkinson's disease results in loss of dopaminergic innervation to the striatum (and other basal ganglia) and a cascade of subsequent consequences. Atrophy of the striatum is also involved in Huntington's disease, choreas, choreoathetosis, and dyskinesias.[15] It is also thought that addiction involves plasticity at striatal synapses.

Bipolar disorder[edit]

There is an association between striatal expression of the PDE10A gene and some bipolar disorder I patients.[16]

History[edit]

In the seventeenth and eighteenth centuries, the term "corpus striatum" was used to designate many distinct, deep, infracortical elements of the hemisphere.[17] In 1941, Cécile and Oskar Vogt simplified the nomenclature by proposing the term striatum for all elements built with striatal elements (see primate basal ganglia system): the caudate, the putamen, and the fundus striati, that ventral part linking the two preceding together ventrally to the inferior part of the internal capsule.

The term neostriatum was forged 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.[18]

See also[edit]

References[edit]

  1. ^ "DBS: The Basal Ganglia". 
  2. ^ Rolls, Edmund (Aug–Sep 1994). "Neurophysiology and cognitive functions of the striatum.". Révue Neurologique 150 (8–9): 648–60. PMID 7754303. 
  3. ^ a b Tepper JM, Tecuapetla F, Koós T, Ibáñez-Sandoval O. Front Neuroanat. 2010 Dec 29;4:150. doi: 10.3389/fnana.2010.00150. PMID 21228905
  4. ^ Goldberg JA, Reynolds JN. Neuroscience. 2011 Dec 15;198:27–43. doi: 10.1016/j.neuroscience.2011.08.067. Epub 2011 Sep 8. Review. PMID 21925242
  5. ^ Morris G, Arkadir D, Nevet A, Vaadia E, Bergman H. Neuron. 2004 Jul 8;43(1):133-43. PMID 15233923
  6. ^ Koós T, Tepper JM. Nat Neurosci. 1999 May;2(5):467-72. PMID 10321252
  7. ^ Ibáñez-Sandoval O, Tecuapetla F, Unal B, Shah F, Koós T, Tepper JM. J Neurosci. 2010 May 19;30(20):6999–7016. doi: 10.1523/JNEUROSCI.5996-09.2010. PMID 20484642
  8. ^ Ibáñez-Sandoval O, Tecuapetla F, Unal B, Shah F, Koós T, Tepper JM. J Neurosci. 2011 Nov 16;31(46):16757-69. doi: 10.1523/JNEUROSCI.2628-11.2011. PMID 22090502
  9. ^ English DF, Ibanez-Sandoval O, Stark E, Tecuapetla F, Buzsáki G, Deisseroth K, Tepper JM, Koos T. Nat Neurosci. 2011 Dec 11;15(1):123-30. doi: 10.1038/nn.2984. PMID 22158514
  10. ^ "Neuron-generating brain region could hold promise for neurodegenerative therapies". Science Daily. February 20, 2014. Retrieved February 24, 2014. 
  11. ^ Rosell A, Giménez-Amaya JM (1999). "Anatomical re-evaluation of the corticostriatal projections to the caudate nucleus: a retrograde labeling study in the cat". Neurosci Res 34 (4): 257–69. doi:10.1016/S0168-0102(99)00060-7. PMID 10576548. 
  12. ^ Voytek, Bradley; Knight, Robert T. (19 October 2010). "Prefrontal cortex and basal ganglia contributions to working memory". Proceedings of the National Academy of Sciences of the United States of America 107 (42): 18167=18172. doi:10.1073/pnas.1007277107. 
  13. ^ LUNA, BEATRIZ; SWEENEY, JOHN A. (1 June 2004). "The Emergence of Collaborative Brain Function: fMRI Studies of the Development of Response Inhibition". Annals of the New York Academy of Sciences 1021 (1): 296–309. doi:10.1196/annals.1308.035. 
  14. ^ "Department of Physiology, Development and Neuroscience: About the Department". 
  15. ^ Walker FO (January 2007). "Huntington's disease". Lancet 369 (9557): 218–28. doi:10.1016/S0140-6736(07)60111-1. PMID 17240289. 
  16. ^ Science Daily: Scientists pinpoint gene variations linked to higher risk of bipolar disorder
  17. ^ Raymond Vieussens, 1685
  18. ^ Neostriatum at the US National Library of Medicine Medical Subject Headings (MeSH)

External links[edit]