Brain dopamine‐stimulated adenylyl cyclase activity in Parkinson's disease, multiple system atrophy, and progressive supranuclear palsy
Identifieur interne : 002C84 ( Main/Exploration ); précédent : 002C83; suivant : 002C85Brain dopamine‐stimulated adenylyl cyclase activity in Parkinson's disease, multiple system atrophy, and progressive supranuclear palsy
Auteurs : Junchao Tong [Canada] ; Paul S. Fitzmaurice ; Lee Cyn Ang [Royaume-Uni] ; Yoshiaki Furukawa [Canada] ; Mark Guttman ; Stephen J. KishSource :
- Annals of Neurology [ 0364-5134 ] ; 2004-01.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Adenylyl Cyclases (metabolism), Aged, Aged, 80 and over, Brain (metabolism), Brain (pathology), Dopamine, Dopamine (metabolism), Enzyme Activation (physiology), Female, Humans, Male, Middle Aged, Multiple System Atrophy (physiopathology), Multiple system atrophy, Nervous system diseases, Paralysis, Parkinson Disease (physiopathology), Parkinson disease, Receptors, Dopamine D1 (metabolism), Supranuclear Palsy, Progressive (physiopathology).
- MESH :
- chemical , metabolism : Adenylyl Cyclases, Dopamine, Receptors, Dopamine D1.
- metabolism : Brain.
- pathology : Brain.
- physiology : Enzyme Activation.
- physiopathology : Multiple System Atrophy, Parkinson Disease, Supranuclear Palsy, Progressive.
- Aged, Aged, 80 and over, Female, Humans, Male, Middle Aged.
Abstract
The dopamine D1 receptor is considered to participate in levodopa's antiparkinsonian action and levodopa‐induced dyskinesias. We examined the functional status of the D1 receptor in brain of patients with Parkinson's disease (PD), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). Dopamine‐stimulated adenylyl cyclase activity was significantly increased in putamen (+43%) and frontal cortex (+52%) in PD, normal in PSP, but decreased by 47% in putamen in MSA. The supersensitive dopamine D1 receptors in both striatum and cerebral cortex in PD might compensate for dopamine deficiency, but could also contribute to long‐term complications of levodopa therapy.
Url:
DOI: 10.1002/ana.10814
Affiliations:
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Le document en format XML
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Kish</name><affiliation><wicri:noCountry code="subField">Toronto</wicri:noCountry></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of Neurology</title><title level="j" type="sub">Official Journal of the American Neurological Association and the Child Neurology Society</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="ISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2004-01">2004-01</date><biblScope unit="volume">55</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="125">125</biblScope><biblScope unit="page" to="129">129</biblScope></imprint><idno type="ISSN">0364-5134</idno></series><idno type="istex">E3DB5418B70EF47DF03B2C9C92DD2597C2E3540B</idno><idno type="DOI">10.1002/ana.10814</idno><idno type="ArticleID">ANA10814</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0364-5134</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenylyl Cyclases (metabolism)</term><term>Aged</term><term>Aged, 80 and over</term><term>Brain (metabolism)</term><term>Brain (pathology)</term><term>Dopamine</term><term>Dopamine (metabolism)</term><term>Enzyme Activation (physiology)</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Multiple System Atrophy (physiopathology)</term><term>Multiple system atrophy</term><term>Nervous system diseases</term><term>Paralysis</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson disease</term><term>Receptors, Dopamine D1 (metabolism)</term><term>Supranuclear Palsy, Progressive (physiopathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Adenylyl Cyclases</term><term>Dopamine</term><term>Receptors, Dopamine D1</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Brain</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Enzyme Activation</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Multiple System Atrophy</term><term>Parkinson Disease</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>Middle Aged</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Atrophie multisystématisée</term><term>Dopamine</term><term>Paralysie</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 dopamine D1 receptor is considered to participate in levodopa's antiparkinsonian action and levodopa‐induced dyskinesias. We examined the functional status of the D1 receptor in brain of patients with Parkinson's disease (PD), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). Dopamine‐stimulated adenylyl cyclase activity was significantly increased in putamen (+43%) and frontal cortex (+52%) in PD, normal in PSP, but decreased by 47% in putamen in MSA. The supersensitive dopamine D1 receptors in both striatum and cerebral cortex in PD might compensate for dopamine deficiency, but could also contribute to long‐term complications of levodopa therapy.</div></front></TEI><affiliations><list><country><li>Canada</li><li>Royaume-Uni</li></country><region><li>Angleterre</li><li>Grand Londres</li></region><settlement><li>Londres</li></settlement></list><tree><noCountry><name sortKey="Fitzmaurice, Paul S" sort="Fitzmaurice, Paul S" uniqKey="Fitzmaurice P" first="Paul S." last="Fitzmaurice">Paul S. Fitzmaurice</name><name sortKey="Guttman, Mark" sort="Guttman, Mark" uniqKey="Guttman M" first="Mark" last="Guttman">Mark Guttman</name><name sortKey="Kish, Stephen J" sort="Kish, Stephen J" uniqKey="Kish S" first="Stephen J." last="Kish">Stephen J. Kish</name></noCountry><country name="Canada"><noRegion><name sortKey="Tong, Junchao" sort="Tong, Junchao" uniqKey="Tong J" first="Junchao" last="Tong">Junchao Tong</name></noRegion><name sortKey="Furukawa, Yoshiaki" sort="Furukawa, Yoshiaki" uniqKey="Furukawa Y" first="Yoshiaki" last="Furukawa">Yoshiaki Furukawa</name></country><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Ang, Lee Cyn" sort="Ang, Lee Cyn" uniqKey="Ang L" first="Lee Cyn" last="Ang">Lee Cyn Ang</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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