Academic literature on the topic 'Interneurones striataux'
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Journal articles on the topic "Interneurones striataux"
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Xu, Meiyu, Andrew Kobets, Jung-Chieh Du, Jessica Lennington, Lina Li, Mounira Banasr, Ronald S. Duman, Flora M. Vaccarino, Ralph J. DiLeone, and Christopher Pittenger. "Targeted ablation of cholinergic interneurons in the dorsolateral striatum produces behavioral manifestations of Tourette syndrome." Proceedings of the National Academy of Sciences 112, no. 3 (January 5, 2015): 893–98. http://dx.doi.org/10.1073/pnas.1419533112.
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Gilles de la Tourette syndrome (TS) is characterized by tics, which are transiently worsened by stress, acute administration of dopaminergic drugs, and by subtle deficits in motor coordination and sensorimotor gating. It represents the most severe end of a spectrum of tic disorders that, in aggregate, affect ∼5% of the population. Available treatments are frequently inadequate, and the pathophysiology is poorly understood. Postmortem studies have revealed a reduction in specific striatal interneurons, including the large cholinergic interneurons, in severe disease. We tested the hypothesis that this deficit is sufficient to produce aspects of the phenomenology of TS, using a strategy for targeted, specific cell ablation in mice. We achieved ∼50% ablation of the cholinergic interneurons of the striatum, recapitulating the deficit observed in patients postmortem, without any effect on GABAergic markers or on parvalbumin-expressing fast-spiking interneurons. Interneuron ablation in the dorsolateral striatum (DLS), corresponding roughly to the human putamen, led to tic-like stereotypies after either acute stress or d-amphetamine challenge; ablation in the dorsomedial striatum, in contrast, did not. DLS interneuron ablation also led to a deficit in coordination on the rotorod, but not to any abnormalities in prepulse inhibition, a measure of sensorimotor gating. These results support the causal sufficiency of cholinergic interneuron deficits in the DLS to produce some, but not all, of the characteristic symptoms of TS.
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Clarke, Rhona, and Louise Adermark. "Dopaminergic Regulation of Striatal Interneurons in Reward and Addiction: Focus on Alcohol." Neural Plasticity 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/814567.
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Corticobasal ganglia networks coursing through the striatum are key structures for reward-guided behaviors. The ventral striatum (nucleus accumbens (nAc)) and its reciprocal connection with the ventral tegmental area (VTA) represent a primary component of the reward system, but reward-guided learning also involves the dorsal striatum and dopaminergic inputs from the substantia nigra. The majority of neurons in the striatum (>90%) are GABAergic medium spiny neurons (MSNs), but both the input to and the output from these neurons are dynamically controlled by striatal interneurons. Dopamine is a key neurotransmitter in reward and reward-guided learning, and the physiological activity of GABAergic and cholinergic interneurons is regulated by dopaminergic transmission in a complex manner. Here we review the role of striatal interneurons in modulating striatal output during drug reward, with special emphasis on alcohol.
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Rubi, Lena, and Jean-Marc Fritschy. "Increased GABAergic transmission in neuropeptide Y-expressing neurons in the dopamine-depleted murine striatum." Journal of Neurophysiology 123, no. 4 (April 1, 2020): 1496–503. http://dx.doi.org/10.1152/jn.00059.2020.
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As the main input nucleus of the basal ganglia, the striatum plays a central role in planning, control, and execution of movement and motor skill learning. More than 90% of striatal neurons, so-called medium spiny neurons (MSN), are GABAergic projection neurons, innervating primarily the substantia nigra pars reticulata or the globus pallidus internus. The remaining neurons are GABAergic and cholinergic interneurons, synchronizing and controlling striatal output by reciprocal connections with MSN. Besides prominent local cholinergic influence, striatal function is globally regulated by dopamine (DA) from the nigrostriatal pathway. Little is known about whether DA depletion, as occurs in Parkinson’s disease, affects the activity of striatal interneurons. Here we focused on neuropeptide Y (NPY)-expressing interneurons, which are among the major subgroups of GABAergic interneurons in the striatum. We investigated the effects of striatal DA depletion on GABAergic transmission in NPY interneurons by electrophysiologically recording GABAergic spontaneous (s) and miniature (m) inhibitory postsynaptic currents (IPSCs) in identified NPY interneurons in slices from 6-hydroxydopamine (6-OHDA)- and vehicle-injected transgenic NPY-humanized Renilla green fluorescent protein (hrGFP) mice with the whole cell patch-clamp technique. We report a significant increase in sIPSC and mIPSC frequency as well as the occurrence of giant synaptic and burst sIPSCs in the 6-OHDA group, suggesting changes in GABAergic circuit activity and synaptic transmission. IPSC kinetics remained unchanged, pointing to mainly presynaptic changes in GABAergic transmission. These results show that chronic DA depletion following 6-OHDA injection causes activity-dependent and -independent increase of synaptic GABAergic inhibition onto striatal NPY interneurons, confirming their involvement in the functional impairments of the DA-depleted striatum. NEW & NOTEWORTHY Neuropeptide Y (NPY) interneurons regulate the function of striatal projection neurons and are upregulated upon dopamine depletion in the striatum. Here we investigated how dopamine depletion affects NPY circuits and show electrophysiologically that it leads to the occurrence of giant synaptic and burst GABAergic spontaneous inhibitory postsynaptic currents (IPSCs) and to an activity-independent increase in GABAergic miniature IPSC frequency in NPY neurons. We suggest that degeneration of dopaminergic terminals in the striatum causes functional changes in striatal GABAergic function.
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Semba, K., H. C. Fibiger, and S. R. Vincent. "Neurotransmitters in the Mammalian Striatum: Neuronal Circuits and Heterogeneity." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 14, S3 (August 1987): 386–94. http://dx.doi.org/10.1017/s0317167100037781.
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ABSTRACT:The major input and output pathways of the mammalian striatum have been well established. Recent studies have identified a number of neurotransmitters used by these pathways as well as by striatal interneurons, and have begun to unravel their synaptic connections. The major output neurons have been identified as medium spiny neurons which contain ɣ-aminobutyric acid (GABA), endogeneous opioids, and substance P. These neurons project to the pallidum and substantia nigra in a topographic and probably chemically organized manner. The major striatal afferents from the cerebral cortex, thalamus, and substantia nigra terminate, at least in part, on these striatal projection neurons. Striatal interneurons contain acetylcholine, GABA, and somatostatin plus neuropeptide Y, and appear to synapse on striatal projection neurons. In recent years, much activity has been directed to the neurochemical and hodological heterogeneities which occur at a macroscopic level in the striatum. This has led to the concept of a patch-matrix organization in the striatum.
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Poppi, Lauren A., Khue Tu Ho-Nguyen, Anna Shi, Cynthia T. Daut, and Max A. Tischfield. "Recurrent Implication of Striatal Cholinergic Interneurons in a Range of Neurodevelopmental, Neurodegenerative, and Neuropsychiatric Disorders." Cells 10, no. 4 (April 15, 2021): 907. http://dx.doi.org/10.3390/cells10040907.
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Cholinergic interneurons are “gatekeepers” for striatal circuitry and play pivotal roles in attention, goal-directed actions, habit formation, and behavioral flexibility. Accordingly, perturbations to striatal cholinergic interneurons have been associated with many neurodevelopmental, neurodegenerative, and neuropsychiatric disorders. The role of acetylcholine in many of these disorders is well known, but the use of drugs targeting cholinergic systems fell out of favor due to adverse side effects and the introduction of other broadly acting compounds. However, in response to recent findings, re-examining the mechanisms of cholinergic interneuron dysfunction may reveal key insights into underlying pathogeneses. Here, we provide an update on striatal cholinergic interneuron function, connectivity, and their putative involvement in several disorders. In doing so, we aim to spotlight recurring physiological themes, circuits, and mechanisms that can be investigated in future studies using new tools and approaches.
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Ying, Guoxin, Sen Wu, Ruiqing Hou, Wei Huang, Mario R. Capecchi, and Qiang Wu. "The Protocadherin Gene Celsr3 Is Required for Interneuron Migration in the Mouse Forebrain." Molecular and Cellular Biology 29, no. 11 (March 30, 2009): 3045–61. http://dx.doi.org/10.1128/mcb.00011-09.
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ABSTRACT Interneurons are extremely diverse in the mammalian brain and provide an essential balance for functional neural circuitry. The vast majority of murine cortical interneurons are generated in the subpallium and migrate tangentially over a long distance to acquire their final positions. By using a mouse line with a deletion of the Celsr3 (Flamingo, or Fmi1) gene and a knock-in of the green fluorescent protein reporter, we find that Celsr3, a member of the nonclustered protocadherin (Pcdh) family, is predominantly expressed in the cortical interneurons in adults and in the interneuron germinal zones in embryos. We show that Celsr3 is crucial for interneuron migration in the developing mouse forebrain. Specifically, in Celsr3 knockout mice, calretinin-positive interneurons are reduced in the developing neocortex, accumulated in the corticostriatal boundary, and increased in the striatum. Moreover, the laminar distribution of cortical calbindin-positive cells is altered. Finally, we found that expression patterns of NRG1 (neuregulin-1) and its receptor ErbB4, which are essential for interneuron migration, are changed in Celsr3 mutants. These results demonstrate that the protocadherin Celsr3 gene is essential for both tangential and radial interneuron migrations in a class-specific manner.
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Beatty, Joseph A., Soomin C. Song, and Charles J. Wilson. "Cell-type-specific resonances shape the responses of striatal neurons to synaptic input." Journal of Neurophysiology 113, no. 3 (February 1, 2015): 688–700. http://dx.doi.org/10.1152/jn.00827.2014.
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Neurons respond to synaptic inputs in cell-type-specific ways. Each neuron type may thus respond uniquely to shared patterns of synaptic input. We applied statistically identical barrages of artificial synaptic inputs to four striatal cell types to assess differences in their responses to a realistic input pattern. Each interneuron type fired in phase with a specific input-frequency component. The fast-spiking interneuron fired in relation to the gamma-band (and higher) frequencies, the low-threshold spike interneuron to the beta-band frequencies, and the cholinergic neurons to the delta-band frequencies. Low-threshold spiking and cholinergic interneurons showed input impedance resonances at frequencies matching their spiking resonances. Fast-spiking interneurons showed resonance of input impedance but at lower than gamma frequencies. The spiny projection neuron's frequency preference did not have a fixed frequency but instead tracked its own firing rate. Spiny cells showed no input impedance resonance. Striatal interneurons are each tuned to a specific frequency band corresponding to the major frequency components of local field potentials. Their influence in the circuit may fluctuate along with the contribution of that frequency band to the input. In contrast, spiny neurons may tune to any of the frequency bands by a change in firing rate.
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Partridge, John G., Megan J. Janssen, David Y. T. Chou, Ken Abe, Zofia Zukowska, and Stefano Vicini. "Excitatory and Inhibitory Synapses in Neuropeptide Y–Expressing Striatal Interneurons." Journal of Neurophysiology 102, no. 5 (November 2009): 3038–45. http://dx.doi.org/10.1152/jn.00272.2009.
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Although rare, interneurons are pivotal in governing striatal output by extensive axonal arborizations synapsing on medium spiny neurons. Using a genetically modified mouse strain in which a green fluorescent protein (GFP) is driven to be expressed under control of the neuropeptide Y (NPY) promoter, we identified NPY interneurons and compared them with striatal principal neurons. We found that the bacteria artificial chromosome (BAC)- npy mouse expresses GFP with high fidelity in the striatum to the endogenous expression of NPY. Patch-clamp analysis from NPY neurons showed a heterogeneous population of striatal interneurons. In the majority of cells, we observed spontaneous firing of action potentials in extracellular recordings. On membrane rupture, most NPY interneurons could be classified as low-threshold spiking interneurons and had high-input resistance. Voltage-clamp recordings showed that both GABA and glutamate gated ion channels mediate synaptic inputs onto these striatal interneurons. AMPA receptor–mediated spontaneous excitatory postsynaptic currents (sEPSCs) were small in amplitude and infrequent in NPY neurons. Evoked EPSCs did not show short-term plasticity but some rectification. Evoked N-methyl-d-aspartate (NMDA) EPSCs had fast decay kinetics and were poorly sensitive to an NR2B subunit containing NMDA receptor blocker. Spontaneous inhibitory postsynaptic currents (sIPSCs) were mediated by GABAA receptors and were quite similar among all striatal neurons studied. On the contrary, evoked IPSCs decayed faster in NPY neurons than in other striatal neurons. These data report for the first time specific properties of synaptic transmission to NPY striatal interneurons.
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Seeher, Sandra, Bradley A. Carlson, Angela C. Miniard, Eva K. Wirth, Yassin Mahdi, Dolph L. Hatfield, Donna M. Driscoll, and Ulrich Schweizer. "Impaired selenoprotein expression in brain triggers striatal neuronal loss leading to co-ordination defects in mice." Biochemical Journal 462, no. 1 (July 24, 2014): 67–75. http://dx.doi.org/10.1042/bj20140423.
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Selenoproteins contain the rare amino acid selenocysteine. Reduced selenium levels in the brain lead to a complex neurological phenotype affecting cortical and hippocampal GABAergic interneurons. Here we show that striatal interneuron density is reduced in mice with impaired selenoprotein expression.
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Berg, Allison P., and Douglas A. Bayliss. "Striatal Cholinergic Interneurons Express a Receptor-Insensitive Homomeric TASK-3–Like Background K+ Current." Journal of Neurophysiology 97, no. 2 (February 2007): 1546–52. http://dx.doi.org/10.1152/jn.01090.2006.
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Large aspiny cholinergic interneurons provide the sole source of striatal acetylcholine, a neurotransmitter essential for normal basal ganglia function. Cholinergic interneurons engage in multiple firing patterns that depend on interactions among various voltage-dependent ion channels active at different membrane potentials. Leak conductances, particularly leak K+ channels, are of primary importance in establishing the prevailing membrane potential. We have combined molecular neuroanatomy with whole cell electrophysiology to demonstrate that TASK-3 (K2P9.1, Kcnk9) subunits contribute to leak K+ currents in striatal cholinergic interneurons. Immunostaining for choline acetyltransferase was combined with TASK-3 labeling, using nonradioactive cRNA probes or antisera selective for TASK-3, to demonstrate that striatal cholinergic neurons universally express TASK-3. Consistent with this, we isolated a pH-, anesthetic-, and Zn2+-sensitive current with properties expected of TASK-3 homodimeric channels. Surprisingly, activation of Gαq-linked receptors (metabotropic glutamate mGluR1/5 or histamine H1) did not appear to modulate native interneuron TASK-3–like currents. Together, our data indicate that homomeric TASK-3–like background K+ currents contribute to establishing membrane potential in striatal cholinergic interneurons and they suggest that receptor modulation of TASK channels is dependent on cell context.
Dissertations / Theses on the topic "Interneurones striataux"
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Fino, Elodie. "Transmission et plasticité activité-dépendante au niveau des synapses cortico-striatales." Phd thesis, Université Pierre et Marie Curie - Paris VI, 2007. http://tel.archives-ouvertes.fr/tel-00811483.
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Le striatum a pour rôle de sélectionner et d'intégrer les informations provenant du cortex et ainsi construire et transmettre une réponse adaptée aux stimuli environnementaux. Nous avons caractérisé les propriétés électrophysiologiques des différents neurones du striatum (neurones de sortie, NETM, et interneurones) dans des conditions normales, et lors d'une déplétion de dopamine striatale. Grâce à un modèle de tranche de cerveau de rat dans laquelle les afférences cortico-striatales sont conservées intactes, nous avons mis en évidence une plasticité synaptique bidirectionnelle dans les NETM ainsi qu'une homéostasie puissante au niveau des synapses cortico-striatales. Nous avons ensuite observé que, outre les NETM, le cortex contacte également les interneurones striataux, avec une séquence d'activation particulière et qu'il existe une spécificité cellulaire de la " spike-timing dependent plasticity " (STDP) dans le striatum. Enfin, nous avons mis en évidence que, au niveau des NETM, des signaux sous-liminaires, en coïncidence avec une activité corticale, sont capables d'induire des phénomènes de plasticité synaptique à long-terme.
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Ztaou, Samira. "Implication des interneurones cholinergiques striataux dans la physiopathologie de la maladie de Parkinson : étude optogénétique, pharmacologique et comportementale." Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM4736/document.
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La maladie de Parkinson (MP) est caractérisée par une perte dopaminergique dans le striatum, structure sous-corticale impliquée dans le contrôle moteur, la mémoire et les comportements émotionnels. Les interneurones cholinergiques (ChIs) striataux jouent un rôle clef dans cette réorganisation pathologique du striatum en modulant l’activité des neurones de projection striataux (MSNs). Ce travail vise à étudier l’implication des ChIs et des récepteurs muscariniques (mAChRs) dans les mécanismes qui sous-tendent l’expression des déficits moteurs, cognitifs et émotionnels dans différents modèles de la MP chez la souris. L’inhibition optogénétique des ChIs réduit les déficits moteurs (akinésie, asymétrie posturale, déficit sensori-moteur). Les enregistrements électrophysiologiques montrent que l’inhibition des ChIs réduit l’excitabilité des MSNs et rétablit l’équilibre d’activité des deux voies de sortie striatale. Ces effets antiparkinsoniens sont reproduits par le blocage pharmacologique striatal des mAChRs M1 et M4. Ils sont dus à une action préférentielle de l’ACh sur les mAChRs au niveau des MSNs à l’origine de la voie striatonigrale puisqu’ils disparaissent chez des souris invalidées pour les récepteurs M4 exprimés dans ces neurones. La photoinhibition des ChIs réduit les déficits mnésiques et l’anxiété. L’antagoniste des mAChRs M1 réduit l’anxiété mais est inefficace sur les déficits mnésiques, suggérant que d’autres récepteurs cholinergiques striataux puissent être engagés dans les fonctions mnésiques. L’ensemble de nos résultats apporte un éclairage nouveau sur l’implication des ChIs striataux dans le fonctionnement physiologique et pathologique du striatumParkinson’s disease (PD) is characterized by a dopamiergic loss into the striatum, a subcortical structure involved in motor control, memory and emotional behaviors. Striatal cholinergic interneurons (ChIs) play a key role in this pathological reorganization of the striatal circuitry by modulating striatal projection neurons (MSNs). This study aims to investigate the involvement of ChIs and muscarinic receptors (mAChRs) in the mechanisms underlying the expression of motor, cognitive and emotional deficits observed in different models of PD in mice. ChIs optogenetic inhibition reduced motor deficits (akinesia, postural asymmetry, sensorimotor deficit). Electrophysiological recordings show that ChIs photoinhibition reduces MSNs excitability and restores the balance between the two striatal output pathways. These antiparkinsonian effects are reproduced by pharmacological intrastriatal blockade of M1 and M4 mAChRs. They are due to a preferential action of ACh on mAChRs expressed on striatonigral MSNs since the deficits disappear in mutant mice that lack M4 mAChRs only in these neurons. ChIs photoinhibition also reduces memory deficits and anxiety. M1 mAChRs antagonist reduces anxiety but is inefficient on memory deficits, suggesting that other cholinergic receptors might be involved in striatal memory functions. Overall, these results give new insights on the role of cholinergic interneurons in the normal and pathological functioning of the striatum
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Chabbert, Dorian. "Conséquences de la délétion conditionnelle du gène Tshz3 dans la circuiterie cortico-striée : implications dans les troubles du spectre autistique." Thesis, Aix-Marseille, 2017. http://www.theses.fr/2017AIXM0207.
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Dès les stades précoces du développement et jusqu’à l’âge adulte, le facteur de transcription TSHZ3 est fortement exprimé dans les neurones pyramidaux (PNs) du cortex. Les PNs de la couche V forment la synapse cortico-striée en contactant les neurones épineux moyens (MSNs) du striatum. A ce niveau, l’expression de TSHZ3 n’est pas retrouvée dans les MSNs mais dans les interneurones cholinergiques (CINs). Des données récentes ont établi un lien entre délétion hétérozygote du gène TSHZ3/Tshz3, troubles du spectre autistique (TSA) et dysfonctionnement de la circuiterie cortico-striée (Caubit et al., Nat Genet 2016). Afin de mieux comprendre le rôle de TSHZ3 dans la circuiterie cortico-striée, nous avons caractérisé deux modèles murins de délétion conditionnelle de Tshz3, ciblant soit les neurones de projection à partir de la période postnatale (souris Tshz3-pnCxKO), soit les neurones cholinergiques à partir de la période embryonnaire (souris Tshz3-ChATCre). Chez les souris Tshz3-pnCxKO, la perte de TSHZ3 entraîne une moindre excitabilité des PNs de la couche V, ainsi qu’une diminution de la probabilité de libération du glutamate par leurs afférences. Nous montrons également une profonde altération du fonctionnement de la synapse cortico-striée. Chez les souris Tshz3-ChATCre, nous montrons que la perte de Tshz3 modifie les propriétés membranaires et de décharge d’une proportion des CINs, qui sont les seuls neurones cholinergiques de l'encéphale exprimant TSHZ3 de façon importante. Ces changements fonctionnels suggèrent que TSHZ3 joue un rôle clé dans le développement des PNs du cortex, de la voie cortico-striée et des CINs, confirmant son implication dans les TSAThe zinc-finger transcription factor TSHZ3 is highly expressed by cortical projection neurons (PNs) from embryonic stages to adulthood, including layer V pyramidal neurons that project to the striatum. There, TSHZ3 is expressed by cholinergic interneurons (CINs) but not by the main targets of PNs, i.e. the medium spiny neurons. Interestingly, recent evidences link heterozygous TSHZ3/Tshz3 gene deletion to autism spectrum disorder (ASD) and to corticostrial circuitry dysfunction (Caubit et al., Nat Genet 2016). In order to provide further insights on the role of Tshz3 in the corticostriatal circuitry, we have characterized two conditional KO mouse models in which its expression is lost either in projection neurons at early postnatal stage (Tshz3-pnCxKO) or in cholinergic cells beginning at embryonic stage (Tshz3-ChATCre). In Tshz3-pnCxKO mice, we confirmed that Tshz3 expression is lost in glutamatergic PNs without altering their number. Our electrophysiological study revealed that layer V PNs are less excitable and that glutamate release probability from their afferents is decreased. We also found dramatic changes of both corticostriatal synaptic transmission and plasticity. In ChAT-Cre mice, we found that Tshz3 is expressed in the striatum by almost 100% of CINs, while it is little or no expressed in the other cholinergic nuclei of the brain. Interestingly, the loss of Tshz3 impacts the spontaneous firing pattern of a subpopulation of CINs without altering their number. These functional changes suggest that TSHZ3 plays a key role in PNs, corticostriatal pathway and CINs development, supporting its implication in ASD
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Bell, M. I. "Characterisation of cholinergic interneurones in the rat striatum." Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596535.
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The physiology and pharmacology of rat striatal cholinergic interneurones has been characterised using the whole-cell patch-clamp technique, in situ hybridisation, single cell RT-PCR and dual fluorescence immunocytochemistry. Cholinergic interneurones displayed a characteristic resting electrophysiology. The resting membrane potential was relatively depolarised and was associated with a relatively large input resistance. All neurones showed a characteristic reduction in their voltage-current relationship that corresponded to the hyperpolarisation-activated current (Ih). Action potentials were associated with a relatively long afterhyperpolarisation. Substance P caused a depolarisation in cholinergic interneurones via a NK1 receptor-mediated Ca2+- activated inward current. The inward current was inhibited by the phospholipase C inhibitor U-73122, and by the inclusion of the inositol 1,4,5 triphosphate receptor antagonist heparin in the electrode solution. These findings correlated with gene expression studies showing the presence of NK1 receptors in these cells. The non-selective metabotropic glutamate (mGlu) receptor agonist 1S,3R-APCD caused a depolarisation of interneurones via a group I mGlu receptor-mediated Ca2+-activated inward current. The inward current was carried by two ionic components and could be inhibited by the PLC inhibitor U73122 and the PKC inhibitor chelerythrine. These findings were consistent with gene expression studies showing the presence of mGluR1 and mGluR5 receptors in these cells. In addition, cholinergic interneurones expressed mGluR2 and mGluR7. Intrastriatal stimulation evoked fast synaptic currents that were mediated by NMDA, AMPA and GABAA receptors.
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Petryszyn, Sarah. "Les neurones à calrétinine du striatum : comparaisons inter-espèces et études anatomopathologiques." Doctoral thesis, Université Laval, 2017. http://hdl.handle.net/20.500.11794/28361.
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Chez les primates, les interneurones GABAergiques qui expriment la calrétinine (CR) sont les interneurones les plus abondants du striatum. Pourtant, à ce jour, leur rôle reste encore mal connu. L’utilisation de techniques d’immunohistochimie en association avec des modèles animaux de la maladie de Parkinson, nous a permis de mieux caractériser ces interneurones. Une première série de travaux décrit pour la toute première fois la distribution et la composition neurochimique des interneurones CR+ chez la souris en condition normale. Ces données ont été directement comparées aux caractéristiques des interneurones CR+ chez les primates humains et non humains. Chez la souris, deux types morphologiques d’interneurones CR+ sont présents : l’un petit et l’autre de taille intermédiaire ; ils se répartissent de manière hétérogène dans le striatum dorsal. Chez le singe et l’humain, trois types morphologiques d’interneurones CR+ existent. En effet, en plus d’interneurones CR+ de petite taille et de taille intermédiaire, il existe des interneurones CR+ de grande taille qui appartiennent en majorité à la catégorie des interneurones cholinergiques du striatum. L’utilisation d’un modèle de souris transgénique Drd1a-tdTomato/Drd2-EGFP (D1/D2) a permis de confirmer que les interneurones cholinergiques exprimaient le récepteur à la dopamine (DA) D2 et de démontrer que les interneurones CR+ chez la souris sont dépourvus des récepteurs D1 et D2. Dans une seconde série de travaux, nous avons cherché à savoir comment la distribution et la composition neurochimique des interneurones CR+ étaient affectées dans le modèle murin de la maladie de Parkinson. Du côté de la lésion 6- hydroxydopamine (6-OHDA), les souris présentent une forte dénervation DAergique du striatum, l’une des principales caractéristiques de la maladie de Parkinson. Dans ces circonstances, seule la densité des interneurones CR+ de taille intermédiaire, dont 13 % apparaissent immunoréactifs pour la tyrosine hydroxylase (TH), est significativement diminuée dans le striatum dorsal. Bien que le noyau accumbens (Acb) subisse également une forte baisse de son innervation DAergique induite par la lésion 6-OHDA, les interneurones CR+ présents dans l’Acb, dont certains sont aussi immunoréactifs pour la calbindine (CB), ne sont pas affectés en terme de nombre et de distribution. La troisième série de travaux nous a permis de reproduire ces analyses chez le primate grâce à l’utilisation du modèle animal de la maladie de Parkinson par intoxication au 1-méthyl-4-phényl-1,2,3,6-tétrahydropyridine (MPTP). Les résultats indiquent que la densité des interneurones CR+ de grande taille est fortement accrue dans le striatum des animaux intoxiqués par le MPTP. Cette forte augmentation de la densité des interneurones CR+ de grande taille est couplée à une augmentation significative de la proportion d’interneurones ChAT+/CR+. L’ensemble de ces données suggère fortement que les interneurones striataux CR+ soient sensibles à une diminution de la concentration en DA dans le striatum dorsal, qui caractérise la maladie de Parkinson. Finalement, une quatrième série de travaux nous a permis de découvrir un regroupement de cellules de petite taille et au phénotype D1 au sein même de l’Acb chez la souris D1/D2, suggérant l’existence d’un nouvel îlot de Calleja dans cette région du cerveau.In the primate striatum, GABAergic neurons that express calretinin (CR) are the most abundant interneurons. Their role within this major basal ganglia component is still unknown. Immunohistochemical techniques used in animal models of Parkinson’s disease allowed us to better characterize these interneurons. A first series of studies enabled us to provide the very first description of the distribution and neurochemical phenotype of the CR+ interneurons in mice striatum, under normal condition. Data was compared to similar findings that were gathered in human and non-human primates. In mice, two morphological phenotypes of CR+ interneurons are present: (1) small and (2) medium-sized CR+ interneurons, both distributed in a heterogeneous way within the dorsal striatum. In primates (both human and non-human), three morphological phenotypes of CR+ interneurons are present within the striatum. In addition to small and medium-sized CR+ interneurons, primates display large-sized CR+ interneurons, which mostly belong to the cholinergic interneurons of the striatum. The use of a double transgenic mouse model Drd1a-tdTomato/Drd2-EGFP (D1/D2) confirmed that the cholinergic interneurons express the dopaminergic (DA) receptor D2, while CR+ interneurons are devoid of D1 and D2. In a second study, we investigated how the distribution and the neurochemical phenotype of the CR+ interneurons are affected in the 6-hydroxydopamine (6-OHDA) mouse model of Parkinson’s disease. In the lesioned striatum, these mice displayed a strong DAergic depletion, one of the main hallmarks of Parkinson’s disease. Under these circumstances, only the density of the medium-sized CR+ interneurons, 13 % of which are immunoreactive for the tyrosine hydroxylase (TH), was decreased within the dorsal striatum. In the accumbens nucleus (Acb), the number and distribution pattern of CR+ interneurons, which are also immunoreactive for calbindin (CB), were not affected, despite that the Acb was also significantly depleted in DA. In a third study, the state of the CR+ striatal interneurons was investigated in a simian model of Parkinson’s disease, involving 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) intoxication. Results indicate that the density of the large-sized CR+ interneurons is dramatically increased within the striatum of MPTP-intoxicated animals. This increase goes along with higher proportion of cholinergic interneurons expressing CR. Altogether, our data suggest that the CR+ interneurons are sensitive to a decrease of the DAergic level in the striatum that characterizes Parkinson’s disease. Finally, a detailed analysis of the Acb in the D1/D2 mice allowed us to detect the presence of a novel island of Calleja located within this brain region.
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Garas, Farid. "Structural and functional heterogeneity of striatal interneuron populations." Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:cfa09ed5-63be-40b4-a974-0f0f0c273656.
Full textAbstract:
The striatum is the largest nucleus of the basal ganglia, and acts as a point of convergence for thalamic, cortical and midbrain inputs. It is involved in both motor and associative forms of learning, and is composed of spiny projection neurons (SPNs) whose output along the so-called "direct pathway" and "indirect pathway" is modified by the activity of diverse sets of interneurons. Four "classical" or major classes of striatal interneuron can be identified according to the selective expression of the molecular markers parvalbumin (PV), calretinin (CR), nitric oxide synthase (NOS) or choline acetyltransferase (ChAT). Although the interneurons within a class are generally considered to be homogeneous in form and function, there is emerging evidence that some classes encompass multiple types of neuron, and that the heterogeneity in striatal interneurons extends beyond these four classes. Defining the extent of interneuron heterogeneity is important for understanding how the striatum processes distinct, topographically-organized inputs from the cortex and thalamus in order to govern a wide range of behaviors. To address these issues, a combination of immunofluorescence microscopy and stereological cell counting approaches was used in striatal tissue from rat, mouse and non-human primate. This was supplemented by in vivo recording and juxtacellular labelling of single neurons in rat. A first set of experiments showed that secretagogin (Scgn), a calcium-binding protein, is expressed by a large number of interneurons in the dorsal striatum of rat and primate, but not in the mouse. In all species tested, secretagogin was expressed by a subset of PV+ interneurons and a subset of CR+ interneurons in the dorsal striatum, but also labelled a group of interneurons that did not express any of the classical markers of striatal interneurons. A second set of experiments in the rat demonstrated that the selective co-expression of Scgn by PV+ interneurons delineates two topographically-, physiologically- and morphologically-distinct cell populations. These topographical differences in distribution were largely conserved in the primate caudate/putamen. In rats, PV+/Scgn+ and PV+/Scgn- interneurons differed significantly in their firing rates, firing patterns and phase-locking to cortical oscillations. The axons of PV+/Scgn+ interneurons were more likely to form appositions with the somata of direct pathway SPNs than indirect pathway SPNs, whereas the opposite was true for the axons of PV+/Scgn- interneurons. These two populations of GABAergic interneurons provide a potential substrate through which either of the striatal output pathways can be rapidly and selectively inhibited, and in turn mediate the expression of behavioral routines. A third set of experiments showed that CR+ interneurons of the dorsal striatum can be separated into three populations based on their molecular, topographical and morphological properties. Small-sized ("Type 3") CR+ interneurons co-expressed Scgn and were restricted in their distribution towards the rostro-medial poles of the striatum in both rats and primates. In rats, these neurons also expressed the transcription factor SP8, suggesting that they may be newly generated throughout adulthood. Large-sized, ("Type 1") CR+ interneurons did not express Scgn, but could be further distinguished by their expression of the transcription factor Lhx7. Medium-sized ("Type 2") CR+ interneurons did not express Scgn or Lhx7, and had heterogeneous electrophysiological properties in vivo. The expression of Scgn, but not other classical interneuron markers, identified a group of interneurons that were restricted in their distribution towards the ventro-medial aspects of the dorsal striatum. A fourth set of experiments showed that these neurons are also present in the core and the shell of the nucleus accumbens. Unlike the case of dorsal striatum, however, PV+ interneurons and CR+ interneurons of the nucleus accumbens did not co-express Scgn. Moreover, many of the interneuron populations studied had greater densities in the ventral striatum compared to the dorsal striatum, and had quantifiably strong biases in their distribution towards a variety of axes within both the core and the shell of the nucleus accumbens. These data thus highlight some major differences in the constituent elements of the microcircuits of dorsal striatum and nucleus accumbens. In conclusion, these studies have revealed a great deal of molecular, topographical, electrophysiological and structural heterogeneity within the interneuron populations of the striatum. As several of these interneuron populations were not evenly distributed throughout the striatum, this ultimately suggests that the microcircuit of the striatum is specialized according to regions that differ in their cortical, thalamic and dopaminergic inputs.
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Sizemore, Rachel J., and n/a. "Innervation of cholinergic interneurons in the striatum of the rat." University of Otago. Department of Anatomy & Structural Biology, 2009. http://adt.otago.ac.nz./public/adt-NZDU20090915.155925.
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Cholinergic interneurons are relatively rare neurons in the rat striatum. These sparsely distributed neurons display a synchronous pause in their tonic firing pattern during reward-related learning. It has been hypothesised that a specialised fast-conducting crossed-corticostriatal pathway is involved in synchronising the pause in tonic firing of these interneurons. This study aimed to detail the innervation of cholinergic interneurons by mapping their proximal and distal inputs and to describe the innervation of the crossed-corticostriatal pathway in male Wistar rats. In vivo electrophysiological recording methods were used to label single crossed-corticostriatal neurons but inadequately labeled their axons. Thus, an anterograde neuronal tracing study was conducted. Biotinylated dextran amine (BDA; 1.2 [mu]l) was pressure-injected into the left cerebral hemisphere. Six days later, the rat was perfused-fixed and the brain sectioned. BDA-labelled axons were traced to both the ipsilateral and contralateral striata. Cholinergic interneurons in the right striatum were double-immunolabelled using an optimised protocol including a polyclonal rabbit anti-m2-muscarinic receptor antibody and a monoclonal goat anti-choline acetyltransferase antibody. All sections were processed for transmission electron microscopy. Serial ultrathin sections were montaged and distal (from non BDA-labelled tissue) and proximal synapses were each mapped separately. A reconstructed distal dendrite from a cholinergic interneuron, located 225 [mu]m from the soma, was analysed. It had an average width of 1 .25[mu]m and 0.726 synapses per [mu]m. This was compared to dendrites in the same tissue and from BDA-labelled tissue. Two dendrites were presumed to be distal profiles of either cholinergic or somatostatin interneurons, while the third was thought to belong to another interneuronal cell type. In terms of surface area, there were less somal synapses compared to those made onto the distal dendrite of the cholinergic interneuron. Somal synapse counts were similar to those reported previously from our laboratory, where symmetric synapses were most common. Crossed-corticostriatal BDA-labelled axons were found to course across proximal dendrites and somas of immunolabelled cholinergic interneurons. Varicosities from these axons were found in close proximity to proximal dendrites and somas of cholinergic interneurons. Of all cholinergic interneurons in an adjacent section, 77% showed closely associated proximal varicosities. Of these, 76% of varicosities were associated with the soma, 11% to proximal dendrites and 13% to both locations. Twenty-nine BDA-labeled axons were analysed using transmission electron microscopy. Most were observed making asymmetric synaptic contact with unlabelled spines. In two cases spines were traced to medium spiny projection neurons. Two axon segments were seen touching the proximal regions of separate cholinergic interneurons. At these contact sites interrupted membrane thickenings were observed. It is proposed here that synapses may form at these sites during reward-related learning. However labelling of the contact sites with a postsynaptic marker would be necessary to confirm their synaptic nature. The current study has gathered information about the distal and proximal innervation patterns of these neurons and described the termination pattern of the crossed-corticostriatal pathway in relation to these neurons for the first time. These findings support the crossed-corticostriatal pathway as one possible anatomical substrate for synchronising the pause response on both sides of the brain.
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Kaneko, Satoshi. "Synaptic Integration Mediated by Striatal Cholinergic Interneurons in Basal Ganglia Function." Kyoto University, 2000. http://hdl.handle.net/2433/151448.
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Gazan, Adeline. "Rôle des interneurones somatostatine dans la physiologie striatale :une approche morphologique, électrophysiologique et comportementale." Doctoral thesis, Universite Libre de Bruxelles, 2019. https://dipot.ulb.ac.be/dspace/bitstream/2013/283380/4/these.pdf.
Full textAbstract:
Le système des noyaux de la base possède un rôle essentiel dans de nombreuses fonctions telles que le contrôle et l’apprentissage moteur ainsi que les processus motivationnels et cognitifs. Le striatum constitue la principale structure d’entrée de ce système et peut être subdivisé en une région dorsale, impliquée dans cet apprentissage et ce contrôle moteur, et une partie ventrale, impliquée dans le système de la récompense et donc les processus motivationnels. Le striatum est composé de deux principales catégories de neurones :les neurones épineux de projection (ou « medium-sized spiny neurons », MSN) qui composent la majorité de la structure, et des interneurones. Les interneurones du striatum participent à la modulation de l’activité des neurones épineux, selon un modus operandi propre à chaque population. Les interneurones exprimant la somatostatine, le neuropeptide Y (NPY) et l’enzyme de synthèse de l’oxyde nitrique (nNOS) constituent l’une de ces populations d’interneurones et n’a encore été que brièvement caractérisée d’un point de vue fonctionnel. Notre travail de thèse s’est donc focalisé sur l’étude de la fonction des interneurones somatostatine du striatum par une approche basée sur la perte de fonction. Cette étude fonctionnelle a été réalisée à l’aide d’un modèle de souris ayant subi une ablation spécifique des interneurones somatostatine dans le striatum. Trois principaux types d’analyses ont été réalisés. La première partie du travail s’est intéressée aux fonctions de ces interneurones à l’échelle cellulaire et, plus particulièrement à l’effet de la perte de ces interneurones sur l’activité électrique des MSNs. Nous avons ainsi observé que l’ablation des interneurones somatostatine induit une dépolarisation du potentiel membranaire de repos des MSNs et une augmentation de leur excitabilité, suggérant que de par les différents neurotransmetteurs que ces interneurones libèrent, ceux-ci participent au contrôle de leurs propriétés électrophysiologiques. Le second chapitre, toujours à l’échelle cellulaire et dans ce même contexte de connexion interneurone-MSN, a visé à étudier l’effet de la perte des interneurones somatostatine du striatum sur la morphologie des neurones de projection et ce, au moyen d’une reconstruction 3D. Celle-ci a mis en évidence que les MSNs présentent une réduction de leur densité d’épines dendritiques dans la portion distale, pouvant être le résultat d’un mécanisme d’homéostasie synaptique, alors que l’arborisation dendritique-même n’est pas modifiée. Finalement, la dernière partie a considéré le rôle des interneurones à une échelle systémique, en étudiant l’effet de l’ablation sur le comportement de la souris. Nous avons observé que l’ablation des interneurones somatostatine striataux n’altère pas le comportement moteur, le comportement nociceptif ou les comportements modélisant l’anxiété ou la dépression mais résulte en une augmentation de l’hyperlocomotion induite par la cocaïne. Il s’est également avéré que le rôle des interneurones somatostatine du striatum dans la réponse à la cocaïne se limite exclusivement à l’aspect locomoteur de la cocaïne et non à l’aspect motivationnel, comme montré par un test de préférence de place conditionné. Des analyses d’expression de différents marqueurs dopaminergiques ont, de plus, permis de suggérer que le phénotype hyperlocomoteur observé impliquerait une augmentation de l’expression du transporteur de la dopamine. Enfin, une étude électrophysiologique et morphologique des MSNs, chez des souris dépourvues d’interneurones somatostatine dans le striatum et sensibilisées à la cocaïne, a permis de mettre en évidence une occlusion des effets de la cocaïne sur les propriétés membranaires passives et l’excitabilité des MSNs. De plus, l’addition de dopamine au milieu extracellulaire induit une augmentation de l’excitabilité des MSNs des souris ayant subi une ablation des interneurones somatostatine striataux, compatible avec l’expression accrue de transporteur de la dopamine. D’autre part, l’étude morphologique a mis en évidence un effet de la sensibilisation à la cocaïne sur la densité des épines proximales des MSNs des souris dépourvues d’interneurones somatostatine.En conclusion, ce travail de thèse a permis de fournir, à l’aide d’un modèle d’ablation spécifique, des données substantielles quant au rôle des interneurones somatostatine du striatum dans la physiologie striatale et, en particulier leur fonction inhibitrice des MSNs, ainsi que leur rôle dans les comportements impliquant le striatum, dont la réponse induite par la cocaïne.Doctorat en Sciences biomédicales et pharmaceutiques (Médecine)
info:eu-repo/semantics/nonPublished
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Du, Zhuowei. "Caractérisation of GABAergic neurotransmission within basal ganglia circuit in R6/1 Huntington's disease mouse model." Thesis, Bordeaux, 2014. http://www.theses.fr/2014BORD0046/document.
Full textAbstract:
Nous avons étudié les récepteurs GABAA dans un modèle de la maladie de Huntington. En combinant des approches biochimiques, moléculaires, électrophysiologiques et de l’imagerie haute résolution, nous avons montré une modification de la neurotransmission GABAergique chez des animaux à des stades pre- et post-symptomatiques. Nos études montrent une diminution de de la neurotransmission GABAergique dans le globus pallidus des souris Huntington qui pourrait conduire à une modification des noyaux de sortie des ganglions de la base et de l’activité motrice. L’ensemble de nos résultats permet de définir le rôle de différents types de récepteurs GABAA dans le cerveau dans des conditions physiologiques et pathologiquesWe explored GABAergic neurotransmission in a mouse model of Huntington's disease. Combining molecular, imaging and electrophysiologicaltechniques, we showed changes of GABAergic neurotransmission in presymptomatic and symptomatic R6/1 mice. Our data demonstrated a decreased GABAergic inhibition in the globus pallidus of R6/1 mice, which could result in an alteration of basal ganglia output nuclei and motor activity. Taken together, our results will help to define the contribution of receptor subtypes to inhibitory transmission throughout the brain in physiological and pathophysiological states
Books on the topic "Interneurones striataux"
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E. H. S. Van Vulpen. The development of rat striatal cholinergic interneurons: Mechanisms important in location and maturation. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1998.
Find full textBook chapters on the topic "Interneurones striataux"
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Miura, Masami, Takeo Suzuki, and Toshihiko Aosaki. "Dopaminergic Regulation of Synaptic Plasticity of Striatal Cholinergic Interneurons." In Catecholamine Research, 191–94. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4757-3538-3_44.
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Aosaki, Toshihiko. "Actions of Dopamine on the Rat Striatal Cholinergic Interneurons." In Advances in Behavioral Biology, 489–97. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0179-4_49.
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French, Sarah Jane, and Henrike Hartung. "Nitrergic Tone Influences Activity of Both Ventral Striatum Projection Neurons and Interneurons." In Advances in Behavioral Biology, 337–47. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0340-2_26.
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Bonsi, Paola, Massimo Tolu, Franco Lavaroni, Giorgio Bernardi, Paolo Calabresi, and Antonio Pisani. "Short and Long Term Modulation of Synaptic Activity in Striatal Cholinergic Interneurons." In The Basal Ganglia VIII, 91–97. Boston, MA: Springer US, 2005. http://dx.doi.org/10.1007/0-387-28066-9_8.
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Doig, Natalie M., and J. Paul Bolam. "Microcircuits of the Striatum." In Handbook of Brain Microcircuits, edited by Gordon M. Shepherd and Sten Grillner, 121–32. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190636111.003.0011.
Full textAbstract:
The striatum (or caudate-putamen, or caudate nucleus and putamen in those species in which they are divided by the internal capsule) is the major division of the basal ganglia, a group of structures involved in a variety of processes, including movement and cognitive and mnemonic functions. The striatum consists of a population of principal neurons, the medium-sized, densely spiny neurons (MSNs)—accounting for up to 97% of all neurons depending on species—which are the projection neurons of the striatum, several populations of GABAergic interneurons, and a population of cholinergic interneurons. The principal afferents of the striatum are glutamatergic, are derived from the cortex and thalamus, and mainly innervate the spines of MSNs. The essential computation performed by the striatum is the decision about which MSNs will fire, the consequence of which is altered firing of basal ganglia output neurons, and hence the selection of the basal ganglia–associated behavior.
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Tepper, James M. "GABAergic Interneurons of the Striatum." In Handbook of Behavioral Neuroscience, 151–66. Elsevier, 2010. http://dx.doi.org/10.1016/b978-0-12-374767-9.00008-1.
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Tepper, J. M., and T. Koós. "GABAergic Interneurons of the Striatum." In Handbook of Behavioral Neuroscience, 157–78. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-802206-1.00008-8.
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Goldberg, Joshua A., and Charles J. Wilson. "The Cholinergic Interneurons of the Striatum." In Handbook of Behavioral Neuroscience, 133–49. Elsevier, 2010. http://dx.doi.org/10.1016/b978-0-12-374767-9.00007-x.
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Emson, P. C., S. J. Augood, R. Señaris, R. Guevara Guzman, J. Kishimoto, K. Kadowaki, P. J. Norris, and K. M. Kendrick. "Chapter 10 Chemical signalling and striatal interneurones." In Progress in Brain Research, 155–65. Elsevier, 1993. http://dx.doi.org/10.1016/s0079-6123(08)61344-8.
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Goldberg, J. A., and C. J. Wilson. "The Cholinergic Interneuron of the Striatum." In Handbook of Behavioral Neuroscience, 137–55. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-802206-1.00007-6.
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