The subthalamic nucleus in the context of movement disorders
Identifieur interne : 002C13 ( Main/Exploration ); précédent : 002C12; suivant : 002C14The subthalamic nucleus in the context of movement disorders
Auteurs : Clement Hamani [Canada] ; Jean A. Saint-Cyr [Canada] ; Justin Fraser [États-Unis] ; Michael Kaplitt [États-Unis] ; Andres M. Lozano [Canada]Source :
- Brain [ 0006-8950 ] ; 2004-01.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- AMPA = 2‐aminomethyl‐phenylacetic acid; BG = basal ganglia; CM = centromedian; EPSP = excitatory post‐synaptic potential; GPe = globus pallidus externus; GPi = globus pallidus internus; HFS = high frequency stimulation; IPSP = inhibitory post‐synaptic potential; mGluR = multiple glutamate receptors; MPTP = 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine; NMDA = N‐methyl‐d‐aspartate; Pf = parafascicular; PPN = pedunculopontine nucleus; SNc = substantia nigra compacta; SNr = substantia nigra reticulata; STN = subthalamic nucleus, Animals, Basal ganglion, Humans, Nervous system diseases, Neurons, Efferent (cytology), Neurotransmitter Agents (physiology), Parkinson Disease (physiopathology), Parkinson Disease (therapy), Parkinson disease, Subthalamic Nucleus (anatomy & histology), Subthalamic Nucleus (drug effects), Subthalamic Nucleus (physiopathology), Subthalamic nucleus, subthalamic nucleus; Parkinson’s disease; basal ganglia; deep brain stimulation; movement disorders.
- MESH :
- chemical , physiology : Neurotransmitter Agents.
- anatomy & histology : Subthalamic Nucleus.
- cytology : Neurons, Efferent.
- drug effects : Subthalamic Nucleus.
- physiopathology : Parkinson Disease, Subthalamic Nucleus.
- therapy : Parkinson Disease.
- Animals, Humans.
Abstract
The subthalamic nucleus (STN) has been regarded as an important modulator of basal ganglia output. It receives its major afferents from the cerebral cortex, thalamus, globus pallidus externus and brainstem, and projects mainly to both segments of the globus pallidus, substantia nigra, striatum and brainstem. The STN is essentially composed of projection glutamatergic neurons. Lesions of the STN induce choreiform abnormal movements and ballism on the contralateral side of the body. In animal models of Parkinson’s disease this nucleus may be dysfunctional and neurons may fire in oscillatory patterns that can be closely related to tremor. Both STN lesions and high frequency stimulation ameliorate the major motor symptoms of parkinsonism in humans and animal models of Parkinson’s disease and reverse certain electrophysiological and metabolic consequences of dopamine depletion. These new findings have led to a renewed interest in the STN. The aim of the present article is to review briefly the major anatomical, pharmacological and physiological aspects of the STN, as well as its involvement in the pathophysiology and treatment of Parkinson’s disease.
Url:
DOI: 10.1093/brain/awh029
Affiliations:
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Le document en format XML
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Saint-Cyr</name><affiliation wicri:level="1"><country>Canada</country><wicri:regionArea>Division of Neurosurgery, Toronto Western Hospital, Toronto Western Research Institute, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author><author><name sortKey="Fraser, Justin" sort="Fraser, Justin" uniqKey="Fraser J" first="Justin" last="Fraser">Justin Fraser</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurological Surgery, Weill Medical College of Cornell University and Division of Neurosurgery, Memorial‐Sloan Kettering Cancer Center, New York, NY</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author><author><name sortKey="Kaplitt, Michael" sort="Kaplitt, Michael" uniqKey="Kaplitt M" first="Michael" last="Kaplitt">Michael Kaplitt</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurological Surgery, Weill Medical College of Cornell University and Division of Neurosurgery, Memorial‐Sloan Kettering Cancer Center, New York, NY</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author><author><name sortKey="Lozano, Andres M" sort="Lozano, Andres M" uniqKey="Lozano A" first="Andres M." last="Lozano">Andres M. Lozano</name><affiliation wicri:level="1"><country>Canada</country><wicri:regionArea>Division of Neurosurgery, Toronto Western Hospital, Toronto Western Research Institute, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Brain</title><title level="j" type="abbrev">Brain</title><idno type="ISSN">0006-8950</idno><idno type="eISSN">1460-2156</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2004-01">2004-01</date><biblScope unit="volume">127</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="4">4</biblScope><biblScope unit="page" to="20">20</biblScope></imprint><idno type="ISSN">0006-8950</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0006-8950</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>AMPA = 2‐aminomethyl‐phenylacetic acid; BG = basal ganglia; CM = centromedian; EPSP = excitatory post‐synaptic potential; GPe = globus pallidus externus; GPi = globus pallidus internus; HFS = high frequency stimulation; IPSP = inhibitory post‐synaptic potential; mGluR = multiple glutamate receptors; MPTP = 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine; NMDA = N‐methyl‐d‐aspartate; Pf = parafascicular; PPN = pedunculopontine nucleus; SNc = substantia nigra compacta; SNr = substantia nigra reticulata; STN = subthalamic nucleus</term><term>Animals</term><term>Basal ganglion</term><term>Humans</term><term>Nervous system diseases</term><term>Neurons, Efferent (cytology)</term><term>Neurotransmitter Agents (physiology)</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson Disease (therapy)</term><term>Parkinson disease</term><term>Subthalamic Nucleus (anatomy & histology)</term><term>Subthalamic Nucleus (drug effects)</term><term>Subthalamic Nucleus (physiopathology)</term><term>Subthalamic nucleus</term><term>subthalamic nucleus; Parkinson’s disease; basal ganglia; deep brain stimulation; movement disorders</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Neurotransmitter Agents</term></keywords><keywords scheme="MESH" qualifier="anatomy & histology" xml:lang="en"><term>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Neurons, Efferent</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term><term>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Noyau gris central</term><term>Noyau sousthalamique</term><term>Parkinson maladie</term><term>Système nerveux pathologie</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The subthalamic nucleus (STN) has been regarded as an important modulator of basal ganglia output. It receives its major afferents from the cerebral cortex, thalamus, globus pallidus externus and brainstem, and projects mainly to both segments of the globus pallidus, substantia nigra, striatum and brainstem. The STN is essentially composed of projection glutamatergic neurons. Lesions of the STN induce choreiform abnormal movements and ballism on the contralateral side of the body. In animal models of Parkinson’s disease this nucleus may be dysfunctional and neurons may fire in oscillatory patterns that can be closely related to tremor. Both STN lesions and high frequency stimulation ameliorate the major motor symptoms of parkinsonism in humans and animal models of Parkinson’s disease and reverse certain electrophysiological and metabolic consequences of dopamine depletion. These new findings have led to a renewed interest in the STN. The aim of the present article is to review briefly the major anatomical, pharmacological and physiological aspects of the STN, as well as its involvement in the pathophysiology and treatment of Parkinson’s disease.</div></front></TEI><affiliations><list><country><li>Canada</li><li>États-Unis</li></country><region><li>État de New York</li></region></list><tree><country name="Canada"><noRegion><name sortKey="Hamani, Clement" sort="Hamani, Clement" uniqKey="Hamani C" first="Clement" last="Hamani">Clement Hamani</name></noRegion><name sortKey="Lozano, Andres M" sort="Lozano, Andres M" uniqKey="Lozano A" first="Andres M." last="Lozano">Andres M. Lozano</name><name sortKey="Saint Yr, Jean A" sort="Saint Yr, Jean A" uniqKey="Saint Yr J" first="Jean A." last="Saint-Cyr">Jean A. Saint-Cyr</name></country><country name="États-Unis"><region name="État de New York"><name sortKey="Fraser, Justin" sort="Fraser, Justin" uniqKey="Fraser J" first="Justin" last="Fraser">Justin Fraser</name></region><name sortKey="Kaplitt, Michael" sort="Kaplitt, Michael" uniqKey="Kaplitt M" first="Michael" last="Kaplitt">Michael Kaplitt</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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