Endogenous dopaminergic tone and dopamine agonist action
Identifieur interne : 002C10 ( PascalFrancis/Checkpoint ); précédent : 002C09; suivant : 002C11Endogenous dopaminergic tone and dopamine agonist action
Auteurs : Sarah A. Treseder [Royaume-Uni] ; Lance A. Smith [Royaume-Uni] ; Peter Jenner [Royaume-Uni]Source :
- Movement disorders [ 0885-3185 ] ; 2000.
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Abstract
Dopamine receptor agonists provide symptomatic relief in the early stages of Parkinson's disease, but with disease progression, their efficacy decreases. The reason behind this decrease in effectiveness is unknown, but maximal efficacy may be dependent on endogenous dopaminergic tone to provide stimulation of D1and D2 receptor subtypes. Therefore, we have investigated the effects of the tyrosine hydroxylase inhibitor α-methyl-p-tyrosine (AMPT) on the actions of D1, D2, and D1/D2 agonists and levodopa (L-dopa) in common marmosets treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. Administration of AMPT alone further increased motor disability and decreased locomotor activity. Administration of L-dopa reversed motor disability and increased locomotor activity, and this reversal was not affected by previous AMPT treatment. The D1 agonist A-77636 and the D2 agonist quinpirole reversed motor deficits, but these effects were markedly inhibited by previous AMPT treatment. Administration of quinpirole with A-77636 produced a reversal of motor deficits that was more resistant to AMPT pretreatment than was the effect produced by quinpirole or A-77636 alone. These data suggest that D1 and D2 receptor stimulation are required for dopamine receptor agonists to produce a maximal antiparkinsonian response. The reversal of motor deficits produced by the mixed D1/D2 agonist apomorphine was more resistant to AMPT treatment than that produced by quinpirole or A-77636. However, the motor effects of A-77636 plus quinpirole and of apomorphine were still affected by AMPT treatment. This suggests that loss of tyrosine hydroxylase activity may also alter motor activity through inhibition of endogenous L-dopa or norepinephrine synthesis, because both are also involved in the genesis of motor activity.
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Smith</name><affiliation wicri:level="3"><inist:fA14 i1="01"><s1>Neurodegenerative Disease Research Centre, Guy's, King's, and St. Thomas's School of Biomedical Sciences, King's College London, Guy's Campus</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ></inist:fA14><country>Royaume-Uni</country><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></author><author><name sortKey="Jenner, Peter" sort="Jenner, Peter" uniqKey="Jenner P" first="Peter" last="Jenner">Peter Jenner</name><affiliation wicri:level="3"><inist:fA14 i1="01"><s1>Neurodegenerative Disease Research Centre, Guy's, King's, and St. Thomas's School of Biomedical Sciences, King's College London, Guy's Campus</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ></inist:fA14><country>Royaume-Uni</country><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">00-0481192</idno><date when="2000">2000</date><idno type="stanalyst">PASCAL 00-0481192 INIST</idno><idno type="RBID">Pascal:00-0481192</idno><idno type="wicri:Area/PascalFrancis/Corpus">002B36</idno><idno type="wicri:Area/PascalFrancis/Curation">000185</idno><idno type="wicri:Area/PascalFrancis/Checkpoint">002C10</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Endogenous dopaminergic tone and dopamine agonist action</title><author><name sortKey="Treseder, Sarah A" sort="Treseder, Sarah A" uniqKey="Treseder S" first="Sarah A." last="Treseder">Sarah A. Treseder</name><affiliation wicri:level="3"><inist:fA14 i1="01"><s1>Neurodegenerative Disease Research Centre, Guy's, King's, and St. Thomas's School of Biomedical Sciences, King's College London, Guy's Campus</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ></inist:fA14><country>Royaume-Uni</country><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></author><author><name sortKey="Smith, Lance A" sort="Smith, Lance A" uniqKey="Smith L" first="Lance A." last="Smith">Lance A. Smith</name><affiliation wicri:level="3"><inist:fA14 i1="01"><s1>Neurodegenerative Disease Research Centre, Guy's, King's, and St. Thomas's School of Biomedical Sciences, King's College London, Guy's Campus</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ></inist:fA14><country>Royaume-Uni</country><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></author><author><name sortKey="Jenner, Peter" sort="Jenner, Peter" uniqKey="Jenner P" first="Peter" last="Jenner">Peter Jenner</name><affiliation wicri:level="3"><inist:fA14 i1="01"><s1>Neurodegenerative Disease Research Centre, Guy's, King's, and St. Thomas's School of Biomedical Sciences, King's College London, Guy's Campus</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ></inist:fA14><country>Royaume-Uni</country><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></author></analytic><series><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno><imprint><date when="2000">2000</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult animal</term><term>Agonist</term><term>Antiparkinson agent</term><term>D1 Dopamine receptor</term><term>D2 Dopamine receptor</term><term>Dopamine</term><term>Dopamine agonist</term><term>Enzyme inhibitor</term><term>Levodopa</term><term>Mechanism of action</term><term>Monkey</term><term>Quinpirole</term><term>Treatment</term><term>Tyrosine 3-monooxygenase</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Agoniste</term><term>Récepteur dopaminergique D1</term><term>Récepteur dopaminergique D2</term><term>Antiparkinsonien</term><term>Lévodopa</term><term>Dopamine</term><term>Inhibiteur enzyme</term><term>Tyrosine 3-monooxygenase</term><term>Apomorphine</term><term>Stimulant dopaminergique</term><term>Quinpirole</term><term>Traitement</term><term>Mécanisme action</term><term>Singe</term><term>Animal adulte</term><term>A-77636</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Singe</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Dopamine receptor agonists provide symptomatic relief in the early stages of Parkinson's disease, but with disease progression, their efficacy decreases. The reason behind this decrease in effectiveness is unknown, but maximal efficacy may be dependent on endogenous dopaminergic tone to provide stimulation of D<sub>1</sub>and D<sub>2</sub> receptor subtypes. Therefore, we have investigated the effects of the tyrosine hydroxylase inhibitor α-methyl-p-tyrosine (AMPT) on the actions of D<sub>1</sub>, D<sub>2</sub>, and D<sub>1</sub>/D<sub>2</sub> agonists and levodopa (L-dopa) in common marmosets treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. Administration of AMPT alone further increased motor disability and decreased locomotor activity. Administration of L-dopa reversed motor disability and increased locomotor activity, and this reversal was not affected by previous AMPT treatment. The D<sub>1</sub> agonist A-77636 and the D<sub>2</sub> agonist quinpirole reversed motor deficits, but these effects were markedly inhibited by previous AMPT treatment. Administration of quinpirole with A-77636 produced a reversal of motor deficits that was more resistant to AMPT pretreatment than was the effect produced by quinpirole or A-77636 alone. These data suggest that D<sub>1</sub> and D<sub>2</sub> receptor stimulation are required for dopamine receptor agonists to produce a maximal antiparkinsonian response. The reversal of motor deficits produced by the mixed D<sub>1</sub>/D<sub>2</sub> agonist apomorphine was more resistant to AMPT treatment than that produced by quinpirole or A-77636. However, the motor effects of A-77636 plus quinpirole and of apomorphine were still affected by AMPT treatment. This suggests that loss of tyrosine hydroxylase activity may also alter motor activity through inhibition of endogenous L-dopa or norepinephrine synthesis, because both are also involved in the genesis of motor activity.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0885-3185</s0></fA01><fA03 i2="1"><s0>Mov. disord.</s0></fA03><fA05><s2>15</s2></fA05><fA06><s2>5</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Endogenous dopaminergic tone and dopamine agonist action</s1></fA08><fA11 i1="01" i2="1"><s1>TRESEDER (Sarah A.)</s1></fA11><fA11 i1="02" i2="1"><s1>SMITH (Lance A.)</s1></fA11><fA11 i1="03" i2="1"><s1>JENNER (Peter)</s1></fA11><fA14 i1="01"><s1>Neurodegenerative Disease Research Centre, Guy's, King's, and St. Thomas's School of Biomedical Sciences, King's College London, Guy's Campus</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ></fA14><fA20><s1>804-812</s1></fA20><fA21><s1>2000</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>20953</s2><s5>354000091356830060</s5></fA43><fA44><s0>0000</s0><s1>© 2000 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>40 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>00-0481192</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Movement disorders</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>Dopamine receptor agonists provide symptomatic relief in the early stages of Parkinson's disease, but with disease progression, their efficacy decreases. The reason behind this decrease in effectiveness is unknown, but maximal efficacy may be dependent on endogenous dopaminergic tone to provide stimulation of D<sub>1</sub>and D<sub>2</sub> receptor subtypes. Therefore, we have investigated the effects of the tyrosine hydroxylase inhibitor α-methyl-p-tyrosine (AMPT) on the actions of D<sub>1</sub>, D<sub>2</sub>, and D<sub>1</sub>/D<sub>2</sub> agonists and levodopa (L-dopa) in common marmosets treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. Administration of AMPT alone further increased motor disability and decreased locomotor activity. Administration of L-dopa reversed motor disability and increased locomotor activity, and this reversal was not affected by previous AMPT treatment. The D<sub>1</sub> agonist A-77636 and the D<sub>2</sub> agonist quinpirole reversed motor deficits, but these effects were markedly inhibited by previous AMPT treatment. Administration of quinpirole with A-77636 produced a reversal of motor deficits that was more resistant to AMPT pretreatment than was the effect produced by quinpirole or A-77636 alone. These data suggest that D<sub>1</sub> and D<sub>2</sub> receptor stimulation are required for dopamine receptor agonists to produce a maximal antiparkinsonian response. The reversal of motor deficits produced by the mixed D<sub>1</sub>/D<sub>2</sub> agonist apomorphine was more resistant to AMPT treatment than that produced by quinpirole or A-77636. However, the motor effects of A-77636 plus quinpirole and of apomorphine were still affected by AMPT treatment. 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Londres</li></region><settlement><li>Londres</li></settlement></list><tree><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Treseder, Sarah A" sort="Treseder, Sarah A" uniqKey="Treseder S" first="Sarah A." last="Treseder">Sarah A. Treseder</name></region><name sortKey="Jenner, Peter" sort="Jenner, Peter" uniqKey="Jenner P" first="Peter" last="Jenner">Peter Jenner</name><name sortKey="Smith, Lance A" sort="Smith, Lance A" uniqKey="Smith L" first="Lance A." last="Smith">Lance A. Smith</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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