Alleviation of parkinsonism by antagonism of excitatory amino acid transmission in the medial segment of the globus pallidus in rat and primate
Identifieur interne : 006199 ( Main/Exploration ); précédent : 006198; suivant : 006200Alleviation of parkinsonism by antagonism of excitatory amino acid transmission in the medial segment of the globus pallidus in rat and primate
Auteurs : Jonathan M. Brotchie [Royaume-Uni] ; Mitchell [Royaume-Uni] ; Michael A. Sambrook [Royaume-Uni] ; Alan R. Crossman [Royaume-Uni]Source :
- Movement Disorders [ 0885-3185 ] ; 1991.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Singe.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (pharmacology), Amino Acids (physiology), Animal, Animals, Antagonist, Basal ganglion, Brain Mapping, Callitrichinae, Degenerative disease, Dominance, Cerebral (drug effects), Dominance, Cerebral (physiology), Dose-Response Relationship, Drug, Excitatory amino acid, Excitatory aminoacid, Experimental disease, Extrapyramidal syndrome, Globus Pallidus (drug effects), Globus Pallidus (physiopathology), Globus pallidus, Kynurenic Acid (pharmacology), Kynurenic acid, Male, Monkey, Motor Activity (drug effects), Motor Activity (physiology), Motor Skills (drug effects), Motor Skills (physiology), Nervous system diseases, Neurologic Examination, Neuromediator, Pallidum, Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (physiopathology), Parkinson disease, Parkinson's disease, Pathophysiology, Rat, Rats, Rats, Inbred Strains, Reserpine (pharmacology), Striatal cell, Synaptic Transmission (drug effects), Synaptic Transmission (physiology).
- MESH :
- chemical , pharmacology : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Kynurenic Acid, Reserpine.
- chemical , physiology : Amino Acids.
- chemically induced : Parkinson Disease, Secondary.
- drug effects : Dominance, Cerebral, Globus Pallidus, Motor Activity, Motor Skills, Synaptic Transmission.
- physiology : Dominance, Cerebral, Motor Activity, Motor Skills, Synaptic Transmission.
- physiopathology : Globus Pallidus, Parkinson Disease, Secondary.
- Animals, Brain Mapping, Callitrichinae, Dose-Response Relationship, Drug, Male, Neurologic Examination, Rats, Rats, Inbred Strains.
Abstract
Recent experimental data has made possible the description of the pathophysiological circuitry that mediates parkinsonism. This work has shown that dopamine‐denervated striatal cells discharge abnormally and that this ultimately causes cells in the medial segment of the globus pallidus to become abnormally overactive. The main driving force behind the overactive cells in the medial pallidal segment appears to be excess activity in the afferent pathway to it from the subthalamic nucleus. This pathway is known to use an excitatory amino acid (EAA) as its transmitter. It was therefore hypothesized that local blockade of EAA transmission in the medial segment of the globus pallidus should reverse parkinsonism. This hypothesis was tested in rat and primate models of parkinsonism by the direct injection of the EAA antagonist, kynurenic acid, into the medial segment of the globus pallidus. The results demonstrate that this procedure can reverse parkinsonism in a dose‐dependent manner, and suggest that manipulation of EAA transmission in the medial segment of the globus pallidus may have therapeutic potential for treating parkinsonism.
Url:
DOI: 10.1002/mds.870060208
Affiliations:
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Le document en format XML
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Brotchie</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Experimental Neurology Group, Department of Cell and Structural Biology, University of Manchester, Manchester</wicri:cityArea></affiliation></author><author><name sortKey="Mitchell" sort="Mitchell" uniqKey="Mitchell" last="Mitchell">Mitchell</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Experimental Neurology Group, Department of Cell and Structural Biology, University of Manchester, Manchester</wicri:cityArea></affiliation></author><author><name sortKey="Sambrook, Michael A" sort="Sambrook, Michael A" uniqKey="Sambrook M" first="Michael A." last="Sambrook">Michael A. Sambrook</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Experimental Neurology Group, Department of Cell and Structural Biology, University of Manchester, Manchester</wicri:cityArea></affiliation></author><author><name sortKey="Crossman, Alan R" sort="Crossman, Alan R" uniqKey="Crossman A" first="Alan R." last="Crossman">Alan R. Crossman</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Experimental Neurology Group, Department of Cell and Structural Biology, University of Manchester, Manchester</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1991">1991</date><biblScope unit="vol">6</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="133">133</biblScope><biblScope unit="page" to="138">138</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">A9AD17DA0AE30ECD329FD845693C8D5DEF7E8E4D</idno><idno type="DOI">10.1002/mds.870060208</idno><idno type="ArticleID">MDS870060208</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (pharmacology)</term><term>Amino Acids (physiology)</term><term>Animal</term><term>Animals</term><term>Antagonist</term><term>Basal ganglion</term><term>Brain Mapping</term><term>Callitrichinae</term><term>Degenerative disease</term><term>Dominance, Cerebral (drug effects)</term><term>Dominance, Cerebral (physiology)</term><term>Dose-Response Relationship, Drug</term><term>Excitatory amino acid</term><term>Excitatory aminoacid</term><term>Experimental disease</term><term>Extrapyramidal syndrome</term><term>Globus Pallidus (drug effects)</term><term>Globus Pallidus (physiopathology)</term><term>Globus pallidus</term><term>Kynurenic Acid (pharmacology)</term><term>Kynurenic acid</term><term>Male</term><term>Monkey</term><term>Motor Activity (drug effects)</term><term>Motor Activity (physiology)</term><term>Motor Skills (drug effects)</term><term>Motor Skills (physiology)</term><term>Nervous system diseases</term><term>Neurologic Examination</term><term>Neuromediator</term><term>Pallidum</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson Disease, Secondary (physiopathology)</term><term>Parkinson disease</term><term>Parkinson's disease</term><term>Pathophysiology</term><term>Rat</term><term>Rats</term><term>Rats, Inbred Strains</term><term>Reserpine (pharmacology)</term><term>Striatal cell</term><term>Synaptic Transmission (drug effects)</term><term>Synaptic Transmission (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>Kynurenic Acid</term><term>Reserpine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Amino Acids</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Dominance, Cerebral</term><term>Globus Pallidus</term><term>Motor Activity</term><term>Motor Skills</term><term>Synaptic Transmission</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Dominance, Cerebral</term><term>Motor Activity</term><term>Motor Skills</term><term>Synaptic Transmission</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Globus Pallidus</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Brain Mapping</term><term>Callitrichinae</term><term>Dose-Response Relationship, Drug</term><term>Male</term><term>Neurologic Examination</term><term>Rats</term><term>Rats, Inbred Strains</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Aminoacide excitateur</term><term>Animal</term><term>Antagoniste</term><term>Extrapyramidal syndrome</term><term>Kynurénique acide</term><term>Maladie dégénérative</term><term>Neuromédiateur</term><term>Noyau gris central</term><term>Pallidum</term><term>Parkinson maladie</term><term>Pathologie expérimentale</term><term>Physiopathologie</term><term>Rat</term><term>Singe</term><term>Système nerveux pathologie</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Singe</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Recent experimental data has made possible the description of the pathophysiological circuitry that mediates parkinsonism. This work has shown that dopamine‐denervated striatal cells discharge abnormally and that this ultimately causes cells in the medial segment of the globus pallidus to become abnormally overactive. The main driving force behind the overactive cells in the medial pallidal segment appears to be excess activity in the afferent pathway to it from the subthalamic nucleus. This pathway is known to use an excitatory amino acid (EAA) as its transmitter. It was therefore hypothesized that local blockade of EAA transmission in the medial segment of the globus pallidus should reverse parkinsonism. This hypothesis was tested in rat and primate models of parkinsonism by the direct injection of the EAA antagonist, kynurenic acid, into the medial segment of the globus pallidus. The results demonstrate that this procedure can reverse parkinsonism in a dose‐dependent manner, and suggest that manipulation of EAA transmission in the medial segment of the globus pallidus may have therapeutic potential for treating parkinsonism.</div></front></TEI><affiliations><list><country><li>Royaume-Uni</li></country><region><li>Angleterre</li></region></list><tree><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Brotchie, Jonathan M" sort="Brotchie, Jonathan M" uniqKey="Brotchie J" first="Jonathan M." last="Brotchie">Jonathan M. Brotchie</name></region><name sortKey="Crossman, Alan R" sort="Crossman, Alan R" uniqKey="Crossman A" first="Alan R." last="Crossman">Alan R. Crossman</name><name sortKey="Mitchell" sort="Mitchell" uniqKey="Mitchell" last="Mitchell">Mitchell</name><name sortKey="Sambrook, Michael A" sort="Sambrook, Michael A" uniqKey="Sambrook M" first="Michael A." last="Sambrook">Michael A. Sambrook</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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