Basal ganglia cholinergic and dopaminergic function in progressive supranuclear palsy
Identifieur interne : 002F94 ( Main/Exploration ); précédent : 002F93; suivant : 002F95Basal ganglia cholinergic and dopaminergic function in progressive supranuclear palsy
Auteurs : Naomi M. Warren [Royaume-Uni] ; Margaret A. Piggott [Royaume-Uni] ; Elizabeth Greally [Royaume-Uni] ; Michelle Lake [Royaume-Uni] ; Andrew Lees (neurologue) [Royaume-Uni] ; David J. Burn [Royaume-Uni]Source :
- Movement Disorders [ 0885-3185 ] ; 2007-08-15.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Autoradiography (methods), Azetidines (pharmacokinetics), Basal Ganglia (drug effects), Basal Ganglia (metabolism), Basal Ganglia (radionuclide imaging), Basal ganglion, Dopamine Plasma Membrane Transport Proteins (metabolism), Female, Humans, Iodine Radioisotopes (pharmacokinetics), Male, Nervous system diseases, Nortropanes (pharmacokinetics), Pirenzepine (pharmacokinetics), Postmortem Changes, Receptors, Cholinergic (metabolism), Receptors, Dopamine (metabolism), Supranuclear Palsy, Progressive (metabolism), Supranuclear Palsy, Progressive (pathology), Supranuclear Palsy, Progressive (radionuclide imaging), Tritium (pharmacokinetics), basal ganglia, cholinergic, dopaminergic, progressive supranuclear palsy.
- MESH :
- chemical , metabolism : Dopamine Plasma Membrane Transport Proteins, Receptors, Cholinergic, Receptors, Dopamine.
- chemical , pharmacokinetics : Azetidines, Iodine Radioisotopes, Nortropanes, Pirenzepine, Tritium.
- drug effects : Basal Ganglia.
- metabolism : Basal Ganglia, Supranuclear Palsy, Progressive.
- methods : Autoradiography.
- pathology : Supranuclear Palsy, Progressive.
- radionuclide imaging : Basal Ganglia, Supranuclear Palsy, Progressive.
- Aged, Aged, 80 and over, Female, Humans, Male, Postmortem Changes.
Abstract
Progressive Supranuclear Palsy (PSP) is a progressive neurodegenerative disorder. In contrast to Parkinson's disease (PD) and dementia with Lewy bodies (DLB), replacement therapy with dopaminergic and cholinergic agents in PSP has been disappointing. The neurochemical basis for this is unclear. Our objective was to measure dopaminergic and cholinergic receptors in the basal ganglia of PSP and control brains. We measured, autoradiographically, dopaminergic (dopamine transporter, 125I PE2I and dopamine D2 receptors, 125I epidepride) and cholinergic (nicotinic α4β2 receptors, 125I 5IA85380 and muscarinic M1 receptors, 3H pirenzepine) parameters in the striatum and pallidum of pathologically confirmed PSP cases (n = 15) and controls (n = 32). In PSP, there was a marked loss of dopamine transporter and nicotinic α4β2 binding in the striatum and pallidum, consistent with loss of nigrostriatal neurones. Striatal D2 receptors were increased in the caudate and muscarinic M1 receptors were unchanged compared with controls. These results do not account for the poor response to dopaminergic and cholinergic replacement therapies in PSP, and suggest relative preservation of postsynaptic striatal projection neurones bearing D2/M1 receptors. © 2007 Movement Disorder Society
Url:
DOI: 10.1002/mds.21573
Affiliations:
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Warren</name><affiliation wicri:level="1"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Institute for Ageing and Heath, University of Newcastle upon Tyne, Newcastle upon Tyne</wicri:regionArea><wicri:noRegion>Newcastle upon Tyne</wicri:noRegion></affiliation></author><author><name sortKey="Piggott, Margaret A" sort="Piggott, Margaret A" uniqKey="Piggott M" first="Margaret A." last="Piggott">Margaret A. 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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="2007-08-15">2007-08-15</date><biblScope unit="vol">22</biblScope><biblScope unit="issue">11</biblScope><biblScope unit="page" from="1594">1594</biblScope><biblScope unit="page" to="1600">1600</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">1BC8FD9B9FF157AB7022B2DC10AE2D59F99113EC</idno><idno type="DOI">10.1002/mds.21573</idno><idno type="ArticleID">MDS21573</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Autoradiography (methods)</term><term>Azetidines (pharmacokinetics)</term><term>Basal Ganglia (drug effects)</term><term>Basal Ganglia (metabolism)</term><term>Basal Ganglia (radionuclide imaging)</term><term>Basal ganglion</term><term>Dopamine Plasma Membrane Transport Proteins (metabolism)</term><term>Female</term><term>Humans</term><term>Iodine Radioisotopes (pharmacokinetics)</term><term>Male</term><term>Nervous system diseases</term><term>Nortropanes (pharmacokinetics)</term><term>Pirenzepine (pharmacokinetics)</term><term>Postmortem Changes</term><term>Receptors, Cholinergic (metabolism)</term><term>Receptors, Dopamine (metabolism)</term><term>Supranuclear Palsy, Progressive (metabolism)</term><term>Supranuclear Palsy, Progressive (pathology)</term><term>Supranuclear Palsy, Progressive (radionuclide imaging)</term><term>Tritium (pharmacokinetics)</term><term>basal ganglia</term><term>cholinergic</term><term>dopaminergic</term><term>progressive supranuclear palsy</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine Plasma Membrane Transport Proteins</term><term>Receptors, Cholinergic</term><term>Receptors, Dopamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacokinetics" xml:lang="en"><term>Azetidines</term><term>Iodine Radioisotopes</term><term>Nortropanes</term><term>Pirenzepine</term><term>Tritium</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Basal Ganglia</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Basal Ganglia</term><term>Supranuclear Palsy, Progressive</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Autoradiography</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Supranuclear Palsy, Progressive</term></keywords><keywords scheme="MESH" qualifier="radionuclide imaging" xml:lang="en"><term>Basal Ganglia</term><term>Supranuclear Palsy, Progressive</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Female</term><term>Humans</term><term>Male</term><term>Postmortem Changes</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Noyau gris central</term><term>Système nerveux pathologie</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Progressive Supranuclear Palsy (PSP) is a progressive neurodegenerative disorder. In contrast to Parkinson's disease (PD) and dementia with Lewy bodies (DLB), replacement therapy with dopaminergic and cholinergic agents in PSP has been disappointing. The neurochemical basis for this is unclear. Our objective was to measure dopaminergic and cholinergic receptors in the basal ganglia of PSP and control brains. We measured, autoradiographically, dopaminergic (dopamine transporter, 125I PE2I and dopamine D2 receptors, 125I epidepride) and cholinergic (nicotinic α4β2 receptors, 125I 5IA85380 and muscarinic M1 receptors, 3H pirenzepine) parameters in the striatum and pallidum of pathologically confirmed PSP cases (n = 15) and controls (n = 32). In PSP, there was a marked loss of dopamine transporter and nicotinic α4β2 binding in the striatum and pallidum, consistent with loss of nigrostriatal neurones. Striatal D2 receptors were increased in the caudate and muscarinic M1 receptors were unchanged compared with controls. These results do not account for the poor response to dopaminergic and cholinergic replacement therapies in PSP, and suggest relative preservation of postsynaptic striatal projection neurones bearing D2/M1 receptors. © 2007 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>Royaume-Uni</li></country><region><li>Angleterre</li><li>Grand Londres</li></region><settlement><li>Londres</li></settlement><orgName><li>National Hospital for Neurology and Neurosurgery</li></orgName></list><tree><country name="Royaume-Uni"><noRegion><name sortKey="Warren, Naomi M" sort="Warren, Naomi M" uniqKey="Warren N" first="Naomi M." last="Warren">Naomi M. Warren</name></noRegion><name sortKey="Burn, David J" sort="Burn, David J" uniqKey="Burn D" first="David J." last="Burn">David J. Burn</name><name sortKey="Greally, Elizabeth" sort="Greally, Elizabeth" uniqKey="Greally E" first="Elizabeth" last="Greally">Elizabeth Greally</name><name sortKey="Lake, Michelle" sort="Lake, Michelle" uniqKey="Lake M" first="Michelle" last="Lake">Michelle Lake</name><name sortKey="Lees, Andrew J" sort="Lees, Andrew J" uniqKey="Lees A" first="Andrew J." last="Lees">Andrew Lees (neurologue)</name><name sortKey="Lees, Andrew J" sort="Lees, Andrew J" uniqKey="Lees A" first="Andrew J." last="Lees">Andrew Lees (neurologue)</name><name sortKey="Piggott, Margaret A" sort="Piggott, Margaret A" uniqKey="Piggott M" first="Margaret A." last="Piggott">Margaret A. Piggott</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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