MovDisordV3, PascalFrancis, Corpus, bibRecord, 001E12

Effects of serotonin 5-HT1A agonist in advanced Parkinson's disease

Identifieur interne : 001E12 ( PascalFrancis/Corpus ); précédent : 001E11; suivant : 001E13

Effects of serotonin 5-HT1A agonist in advanced Parkinson's disease

Auteurs : William Bara-Jimenez ; Francesco Bibbiani ; Michael J. Morris ; Tzvetelina Dimitrova ; Abdullah Sherzai ; Maral M. Mouradian ; Thomas N. Chase

Source :

Movement disorders [ 0885-3185 ] ; 2005.

RBID : Pascal:05-0444021

Descripteurs français

Pascal (Inist)
- Système nerveux pathologie, Parkinson maladie, Dyskinésie, Stimulant sérotoninergique, Stade avancé, Récepteur sérotoninergique 5-HT1A, Sérotonine, Dopamine, Lévodopa.

English descriptors

KwdEn :
- 5-HT1A Serotonine receptor, Advanced stage, Dopamine, Dyskinesia, Levodopa, Nervous system diseases, Parkinson disease, Serotonin, Serotonin agonist.

Abstract

Intermittent stimulation of striatal dopaminergic receptors seems to contribute to motor dysfunction in advanced Parkinson's disease (PD). With severe dopaminergic denervation, exogenous levodopa is largely decarboxylated to dopamine in serotonergic terminals. If 5-HT1A autoreceptors regulate dopamine as well as serotonin release, in parkinsonian patients inhibition of striatal serotonergic neuron firing might help maintain more physiological intrasynaptic dopamine concentrations and thus ameliorate motor fluctuations and dyskinesias. To evaluate this hypothesis, effects of a selective 5-HT1A agonist, sarizotan, given orally at 2 and 5 mg twice daily to 18 relatively advanced parkinsonian patients, were compared with baseline placebo function during a 3-week, double-blind, placebo-controlled, proof-of-concept study. Sarizotan alone or with intravenous levodopa had no effect on parkinsonian severity. But at safe and tolerable doses, sarizotan coadministration reduced levodopa-induced dyskinesias and prolonged its antiparkinsonian response (P ≤ 0.05). Under the conditions of this study, our findings suggest that 5-HT1A receptor stimulation in levodopa-treated parkinsonian patients can modulate striatal dopaminergic function and that 5-HT1A agonists may be useful as levodopa adjuvants in the treatment of PD.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

A01	`01`	`1`		`@0 0885-3185`
A03		`1`		`@0 Mov. disord.`
A05				`@2 20`
A06				`@2 8`
A08	`01`	`1`	`ENG`	`@1 Effects of serotonin 5-HT1A agonist in advanced Parkinson's disease`
A11	`01`	`1`		`@1 BARA-JIMENEZ (William)`
A11	`02`	`1`		`@1 BIBBIANI (Francesco)`
A11	`03`	`1`		`@1 MORRIS (Michael J.)`
A11	`04`	`1`		`@1 DIMITROVA (Tzvetelina)`
A11	`05`	`1`		`@1 SHERZAI (Abdullah)`
A11	`06`	`1`		`@1 MOURADIAN (Maral M.)`
A11	`07`	`1`		`@1 CHASE (Thomas N.)`
A14	`01`			`@1 Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health @2 Bethesda, Maryland @3 USA @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 4 aut. @Z 5 aut. @Z 6 aut. @Z 7 aut.`
A20				`@1 932-936`
A21				`@1 2005`
A23	`01`			`@0 ENG`
A43	`01`			`@1 INIST @2 20953 @5 354000132711360030`
A44				`@0 0000 @1 © 2005 INIST-CNRS. All rights reserved.`
A45				`@0 32 ref.`
A47	`01`	`1`		`@0 05-0444021`
A60				`@1 P`
A61				`@0 A`
A64	`01`	`1`		`@0 Movement disorders`
A66	`01`			`@0 USA`
C01	`01`		`ENG`	@0 Intermittent stimulation of striatal dopaminergic receptors seems to contribute to motor dysfunction in advanced Parkinson's disease (PD). With severe dopaminergic denervation, exogenous levodopa is largely decarboxylated to dopamine in serotonergic terminals. If 5-HT1A autoreceptors regulate dopamine as well as serotonin release, in parkinsonian patients inhibition of striatal serotonergic neuron firing might help maintain more physiological intrasynaptic dopamine concentrations and thus ameliorate motor fluctuations and dyskinesias. To evaluate this hypothesis, effects of a selective 5-HT1A agonist, sarizotan, given orally at 2 and 5 mg twice daily to 18 relatively advanced parkinsonian patients, were compared with baseline placebo function during a 3-week, double-blind, placebo-controlled, proof-of-concept study. Sarizotan alone or with intravenous levodopa had no effect on parkinsonian severity. But at safe and tolerable doses, sarizotan coadministration reduced levodopa-induced dyskinesias and prolonged its antiparkinsonian response (P ≤ 0.05). Under the conditions of this study, our findings suggest that 5-HT1A receptor stimulation in levodopa-treated parkinsonian patients can modulate striatal dopaminergic function and that 5-HT1A agonists may be useful as levodopa adjuvants in the treatment of PD.
C02	`01`	`X`		`@0 002B17`
C02	`02`	`X`		`@0 002B17G`
C02	`03`	`X`		`@0 002B17A03`
C03	`01`	`X`	`FRE`	`@0 Système nerveux pathologie @5 01`
C03	`01`	`X`	`ENG`	`@0 Nervous system diseases @5 01`
C03	`01`	`X`	`SPA`	`@0 Sistema nervioso patología @5 01`
C03	`02`	`X`	`FRE`	`@0 Parkinson maladie @5 02`
C03	`02`	`X`	`ENG`	`@0 Parkinson disease @5 02`
C03	`02`	`X`	`SPA`	`@0 Parkinson enfermedad @5 02`
C03	`03`	`X`	`FRE`	`@0 Dyskinésie @5 03`
C03	`03`	`X`	`ENG`	`@0 Dyskinesia @5 03`
C03	`03`	`X`	`SPA`	`@0 Disquinesia @5 03`
C03	`04`	`X`	`FRE`	`@0 Stimulant sérotoninergique @5 09`
C03	`04`	`X`	`ENG`	`@0 Serotonin agonist @5 09`
C03	`04`	`X`	`SPA`	`@0 Estimulante serotoninérgico @5 09`
C03	`05`	`X`	`FRE`	`@0 Stade avancé @5 10`
C03	`05`	`X`	`ENG`	`@0 Advanced stage @5 10`
C03	`05`	`X`	`SPA`	`@0 Estadio avanzado @5 10`
C03	`06`	`X`	`FRE`	`@0 Récepteur sérotoninergique 5-HT1A @5 11`
C03	`06`	`X`	`ENG`	`@0 5-HT1A Serotonine receptor @5 11 @6 «5-HT1A» Serotonine receptor`
C03	`06`	`X`	`SPA`	`@0 Receptor serotoninérgico 5-HT1A @5 11`
C03	`07`	`X`	`FRE`	`@0 Sérotonine @2 NK @2 FR @5 12`
C03	`07`	`X`	`ENG`	`@0 Serotonin @2 NK @2 FR @5 12`
C03	`07`	`X`	`SPA`	`@0 Serotonina @2 NK @2 FR @5 12`
C03	`08`	`X`	`FRE`	`@0 Dopamine @2 NK @2 FR @5 13`
C03	`08`	`X`	`ENG`	`@0 Dopamine @2 NK @2 FR @5 13`
C03	`08`	`X`	`SPA`	`@0 Dopamina @2 NK @2 FR @5 13`
C03	`09`	`X`	`FRE`	`@0 Lévodopa @2 NK @2 FR @5 14`
C03	`09`	`X`	`ENG`	`@0 Levodopa @2 NK @2 FR @5 14`
C03	`09`	`X`	`SPA`	`@0 Levodopa @2 NK @2 FR @5 14`
C07	`01`	`X`	`FRE`	`@0 Encéphale pathologie @5 37`
C07	`01`	`X`	`ENG`	`@0 Cerebral disorder @5 37`
C07	`01`	`X`	`SPA`	`@0 Encéfalo patología @5 37`
C07	`02`	`X`	`FRE`	`@0 Extrapyramidal syndrome @5 38`
C07	`02`	`X`	`ENG`	`@0 Extrapyramidal syndrome @5 38`
C07	`02`	`X`	`SPA`	`@0 Extrapiramidal síndrome @5 38`
C07	`03`	`X`	`FRE`	`@0 Maladie dégénérative @5 39`
C07	`03`	`X`	`ENG`	`@0 Degenerative disease @5 39`
C07	`03`	`X`	`SPA`	`@0 Enfermedad degenerativa @5 39`
C07	`04`	`X`	`FRE`	`@0 Système nerveux central pathologie @5 40`
C07	`04`	`X`	`ENG`	`@0 Central nervous system disease @5 40`
C07	`04`	`X`	`SPA`	`@0 Sistema nervosio central patología @5 40`
C07	`05`	`X`	`FRE`	`@0 Neurotransmetteur @5 41`
C07	`05`	`X`	`ENG`	`@0 Neurotransmitter @5 41`
C07	`05`	`X`	`SPA`	`@0 Neurotransmisor @5 41`
C07	`06`	`X`	`FRE`	`@0 Catécholamine @5 42`
C07	`06`	`X`	`ENG`	`@0 Catecholamine @5 42`
C07	`06`	`X`	`SPA`	`@0 Catecolamina @5 42`
C07	`07`	`X`	`FRE`	`@0 Mouvement involontaire @5 43`
C07	`07`	`X`	`ENG`	`@0 Involuntary movement @5 43`
C07	`07`	`X`	`SPA`	`@0 Movimiento involuntario @5 43`
C07	`08`	`X`	`FRE`	`@0 Trouble neurologique @5 44`
C07	`08`	`X`	`ENG`	`@0 Neurological disorder @5 44`
C07	`08`	`X`	`SPA`	`@0 Trastorno neurológico @5 44`
N21				`@1 311`
N44	`01`			`@1 OTO`
N82				`@1 OTO`

Format Inist (serveur)

NO :	PASCAL 05-0444021 INIST
ET :	Effects of serotonin 5-HT1A agonist in advanced Parkinson's disease
AU :	BARA-JIMENEZ (William); BIBBIANI (Francesco); MORRIS (Michael J.); DIMITROVA (Tzvetelina); SHERZAI (Abdullah); MOURADIAN (Maral M.); CHASE (Thomas N.)
AF :	Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health/Bethesda, Maryland/Etats-Unis (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut.)
DT :	Publication en série; Niveau analytique
SO :	Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2005; Vol. 20; No. 8; Pp. 932-936; Bibl. 32 ref.
LA :	Anglais
EA :	Intermittent stimulation of striatal dopaminergic receptors seems to contribute to motor dysfunction in advanced Parkinson's disease (PD). With severe dopaminergic denervation, exogenous levodopa is largely decarboxylated to dopamine in serotonergic terminals. If 5-HT1A autoreceptors regulate dopamine as well as serotonin release, in parkinsonian patients inhibition of striatal serotonergic neuron firing might help maintain more physiological intrasynaptic dopamine concentrations and thus ameliorate motor fluctuations and dyskinesias. To evaluate this hypothesis, effects of a selective 5-HT1A agonist, sarizotan, given orally at 2 and 5 mg twice daily to 18 relatively advanced parkinsonian patients, were compared with baseline placebo function during a 3-week, double-blind, placebo-controlled, proof-of-concept study. Sarizotan alone or with intravenous levodopa had no effect on parkinsonian severity. But at safe and tolerable doses, sarizotan coadministration reduced levodopa-induced dyskinesias and prolonged its antiparkinsonian response (P ≤ 0.05). Under the conditions of this study, our findings suggest that 5-HT1A receptor stimulation in levodopa-treated parkinsonian patients can modulate striatal dopaminergic function and that 5-HT1A agonists may be useful as levodopa adjuvants in the treatment of PD.
CC :	002B17; 002B17G; 002B17A03
FD :	Système nerveux pathologie; Parkinson maladie; Dyskinésie; Stimulant sérotoninergique; Stade avancé; Récepteur sérotoninergique 5-HT1A; Sérotonine; Dopamine; Lévodopa
FG :	Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie; Neurotransmetteur; Catécholamine; Mouvement involontaire; Trouble neurologique
ED :	Nervous system diseases; Parkinson disease; Dyskinesia; Serotonin agonist; Advanced stage; 5-HT1A Serotonine receptor; Serotonin; Dopamine; Levodopa
EG :	Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Neurotransmitter; Catecholamine; Involuntary movement; Neurological disorder
SD :	Sistema nervioso patología; Parkinson enfermedad; Disquinesia; Estimulante serotoninérgico; Estadio avanzado; Receptor serotoninérgico 5-HT1A; Serotonina; Dopamina; Levodopa
LO :	INIST-20953.354000132711360030
ID :	05-0444021

Links to Exploration step

Pascal:05-0444021

Le document en format XML

<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en" level="a">Effects of serotonin 5-HT1A agonist in advanced Parkinson's disease</title>
<author><name sortKey="Bara Jimenez, William" sort="Bara Jimenez, William" uniqKey="Bara Jimenez W" first="William" last="Bara-Jimenez">William Bara-Jimenez</name>
<affiliation><inist:fA14 i1="01"><s1>Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health</s1>
<s2>Bethesda, Maryland</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Bibbiani, Francesco" sort="Bibbiani, Francesco" uniqKey="Bibbiani F" first="Francesco" last="Bibbiani">Francesco Bibbiani</name>
<affiliation><inist:fA14 i1="01"><s1>Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health</s1>
<s2>Bethesda, Maryland</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Morris, Michael J" sort="Morris, Michael J" uniqKey="Morris M" first="Michael J." last="Morris">Michael J. Morris</name>
<affiliation><inist:fA14 i1="01"><s1>Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health</s1>
<s2>Bethesda, Maryland</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Dimitrova, Tzvetelina" sort="Dimitrova, Tzvetelina" uniqKey="Dimitrova T" first="Tzvetelina" last="Dimitrova">Tzvetelina Dimitrova</name>
<affiliation><inist:fA14 i1="01"><s1>Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health</s1>
<s2>Bethesda, Maryland</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Sherzai, Abdullah" sort="Sherzai, Abdullah" uniqKey="Sherzai A" first="Abdullah" last="Sherzai">Abdullah Sherzai</name>
<affiliation><inist:fA14 i1="01"><s1>Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health</s1>
<s2>Bethesda, Maryland</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Mouradian, Maral M" sort="Mouradian, Maral M" uniqKey="Mouradian M" first="Maral M." last="Mouradian">Maral M. Mouradian</name>
<affiliation><inist:fA14 i1="01"><s1>Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health</s1>
<s2>Bethesda, Maryland</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Chase, Thomas N" sort="Chase, Thomas N" uniqKey="Chase T" first="Thomas N." last="Chase">Thomas N. Chase</name>
<affiliation><inist:fA14 i1="01"><s1>Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health</s1>
<s2>Bethesda, Maryland</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">INIST</idno>
<idno type="inist">05-0444021</idno>
<date when="2005">2005</date>
<idno type="stanalyst">PASCAL 05-0444021 INIST</idno>
<idno type="RBID">Pascal:05-0444021</idno>
<idno type="wicri:Area/PascalFrancis/Corpus">001E12</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Effects of serotonin 5-HT1A agonist in advanced Parkinson's disease</title>
<author><name sortKey="Bara Jimenez, William" sort="Bara Jimenez, William" uniqKey="Bara Jimenez W" first="William" last="Bara-Jimenez">William Bara-Jimenez</name>
<affiliation><inist:fA14 i1="01"><s1>Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health</s1>
<s2>Bethesda, Maryland</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Bibbiani, Francesco" sort="Bibbiani, Francesco" uniqKey="Bibbiani F" first="Francesco" last="Bibbiani">Francesco Bibbiani</name>
<affiliation><inist:fA14 i1="01"><s1>Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health</s1>
<s2>Bethesda, Maryland</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Morris, Michael J" sort="Morris, Michael J" uniqKey="Morris M" first="Michael J." last="Morris">Michael J. Morris</name>
<affiliation><inist:fA14 i1="01"><s1>Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health</s1>
<s2>Bethesda, Maryland</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Dimitrova, Tzvetelina" sort="Dimitrova, Tzvetelina" uniqKey="Dimitrova T" first="Tzvetelina" last="Dimitrova">Tzvetelina Dimitrova</name>
<affiliation><inist:fA14 i1="01"><s1>Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health</s1>
<s2>Bethesda, Maryland</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Sherzai, Abdullah" sort="Sherzai, Abdullah" uniqKey="Sherzai A" first="Abdullah" last="Sherzai">Abdullah Sherzai</name>
<affiliation><inist:fA14 i1="01"><s1>Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health</s1>
<s2>Bethesda, Maryland</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Mouradian, Maral M" sort="Mouradian, Maral M" uniqKey="Mouradian M" first="Maral M." last="Mouradian">Maral M. Mouradian</name>
<affiliation><inist:fA14 i1="01"><s1>Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health</s1>
<s2>Bethesda, Maryland</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Chase, Thomas N" sort="Chase, Thomas N" uniqKey="Chase T" first="Thomas N." last="Chase">Thomas N. Chase</name>
<affiliation><inist:fA14 i1="01"><s1>Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health</s1>
<s2>Bethesda, Maryland</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
</inist:fA14>
</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="2005">2005</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>5-HT1A Serotonine receptor</term>
<term>Advanced stage</term>
<term>Dopamine</term>
<term>Dyskinesia</term>
<term>Levodopa</term>
<term>Nervous system diseases</term>
<term>Parkinson disease</term>
<term>Serotonin</term>
<term>Serotonin agonist</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Système nerveux pathologie</term>
<term>Parkinson maladie</term>
<term>Dyskinésie</term>
<term>Stimulant sérotoninergique</term>
<term>Stade avancé</term>
<term>Récepteur sérotoninergique 5-HT1A</term>
<term>Sérotonine</term>
<term>Dopamine</term>
<term>Lévodopa</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Intermittent stimulation of striatal dopaminergic receptors seems to contribute to motor dysfunction in advanced Parkinson's disease (PD). With severe dopaminergic denervation, exogenous levodopa is largely decarboxylated to dopamine in serotonergic terminals. If 5-HT1A autoreceptors regulate dopamine as well as serotonin release, in parkinsonian patients inhibition of striatal serotonergic neuron firing might help maintain more physiological intrasynaptic dopamine concentrations and thus ameliorate motor fluctuations and dyskinesias. To evaluate this hypothesis, effects of a selective 5-HT1A agonist, sarizotan, given orally at 2 and 5 mg twice daily to 18 relatively advanced parkinsonian patients, were compared with baseline placebo function during a 3-week, double-blind, placebo-controlled, proof-of-concept study. Sarizotan alone or with intravenous levodopa had no effect on parkinsonian severity. But at safe and tolerable doses, sarizotan coadministration reduced levodopa-induced dyskinesias and prolonged its antiparkinsonian response (P ≤ 0.05). Under the conditions of this study, our findings suggest that 5-HT1A receptor stimulation in levodopa-treated parkinsonian patients can modulate striatal dopaminergic function and that 5-HT1A agonists may be useful as levodopa adjuvants in the treatment of PD.</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>20</s2>
</fA05>
<fA06><s2>8</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG"><s1>Effects of serotonin 5-HT1A agonist in advanced Parkinson's disease</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>BARA-JIMENEZ (William)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>BIBBIANI (Francesco)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>MORRIS (Michael J.)</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>DIMITROVA (Tzvetelina)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>SHERZAI (Abdullah)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>MOURADIAN (Maral M.)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>CHASE (Thomas N.)</s1>
</fA11>
<fA14 i1="01"><s1>Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health</s1>
<s2>Bethesda, Maryland</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
</fA14>
<fA20><s1>932-936</s1>
</fA20>
<fA21><s1>2005</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>20953</s2>
<s5>354000132711360030</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2005 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>32 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>05-0444021</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>Intermittent stimulation of striatal dopaminergic receptors seems to contribute to motor dysfunction in advanced Parkinson's disease (PD). With severe dopaminergic denervation, exogenous levodopa is largely decarboxylated to dopamine in serotonergic terminals. If 5-HT1A autoreceptors regulate dopamine as well as serotonin release, in parkinsonian patients inhibition of striatal serotonergic neuron firing might help maintain more physiological intrasynaptic dopamine concentrations and thus ameliorate motor fluctuations and dyskinesias. To evaluate this hypothesis, effects of a selective 5-HT1A agonist, sarizotan, given orally at 2 and 5 mg twice daily to 18 relatively advanced parkinsonian patients, were compared with baseline placebo function during a 3-week, double-blind, placebo-controlled, proof-of-concept study. Sarizotan alone or with intravenous levodopa had no effect on parkinsonian severity. But at safe and tolerable doses, sarizotan coadministration reduced levodopa-induced dyskinesias and prolonged its antiparkinsonian response (P ≤ 0.05). Under the conditions of this study, our findings suggest that 5-HT1A receptor stimulation in levodopa-treated parkinsonian patients can modulate striatal dopaminergic function and that 5-HT1A agonists may be useful as levodopa adjuvants in the treatment of PD.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B17</s0>
</fC02>
<fC02 i1="02" i2="X"><s0>002B17G</s0>
</fC02>
<fC02 i1="03" i2="X"><s0>002B17A03</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Système nerveux pathologie</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Parkinson maladie</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Dyskinésie</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Dyskinesia</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Disquinesia</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Stimulant sérotoninergique</s0>
<s5>09</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Serotonin agonist</s0>
<s5>09</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Estimulante serotoninérgico</s0>
<s5>09</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Stade avancé</s0>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Advanced stage</s0>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Estadio avanzado</s0>
<s5>10</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Récepteur sérotoninergique 5-HT1A</s0>
<s5>11</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>5-HT1A Serotonine receptor</s0>
<s5>11</s5>
<s6>«5-HT1A» Serotonine receptor</s6>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Receptor serotoninérgico 5-HT1A</s0>
<s5>11</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Sérotonine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>12</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Serotonin</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>12</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Serotonina</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>12</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Dopamine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>13</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Dopamine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>13</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Dopamina</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>13</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Lévodopa</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>14</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Levodopa</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>14</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Levodopa</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>14</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Neurotransmetteur</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Neurotransmitter</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Neurotransmisor</s0>
<s5>41</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Catécholamine</s0>
<s5>42</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Catecholamine</s0>
<s5>42</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Catecolamina</s0>
<s5>42</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Mouvement involontaire</s0>
<s5>43</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Involuntary movement</s0>
<s5>43</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Movimiento involuntario</s0>
<s5>43</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Trouble neurologique</s0>
<s5>44</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Neurological disorder</s0>
<s5>44</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Trastorno neurológico</s0>
<s5>44</s5>
</fC07>
<fN21><s1>311</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
<server><NO>PASCAL 05-0444021 INIST</NO>
<ET>Effects of serotonin 5-HT1A agonist in advanced Parkinson's disease</ET>
<AU>BARA-JIMENEZ (William); BIBBIANI (Francesco); MORRIS (Michael J.); DIMITROVA (Tzvetelina); SHERZAI (Abdullah); MOURADIAN (Maral M.); CHASE (Thomas N.)</AU>
<AF>Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health/Bethesda, Maryland/Etats-Unis (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2005; Vol. 20; No. 8; Pp. 932-936; Bibl. 32 ref.</SO>
<LA>Anglais</LA>
<EA>Intermittent stimulation of striatal dopaminergic receptors seems to contribute to motor dysfunction in advanced Parkinson's disease (PD). With severe dopaminergic denervation, exogenous levodopa is largely decarboxylated to dopamine in serotonergic terminals. If 5-HT1A autoreceptors regulate dopamine as well as serotonin release, in parkinsonian patients inhibition of striatal serotonergic neuron firing might help maintain more physiological intrasynaptic dopamine concentrations and thus ameliorate motor fluctuations and dyskinesias. To evaluate this hypothesis, effects of a selective 5-HT1A agonist, sarizotan, given orally at 2 and 5 mg twice daily to 18 relatively advanced parkinsonian patients, were compared with baseline placebo function during a 3-week, double-blind, placebo-controlled, proof-of-concept study. Sarizotan alone or with intravenous levodopa had no effect on parkinsonian severity. But at safe and tolerable doses, sarizotan coadministration reduced levodopa-induced dyskinesias and prolonged its antiparkinsonian response (P ≤ 0.05). Under the conditions of this study, our findings suggest that 5-HT1A receptor stimulation in levodopa-treated parkinsonian patients can modulate striatal dopaminergic function and that 5-HT1A agonists may be useful as levodopa adjuvants in the treatment of PD.</EA>
<CC>002B17; 002B17G; 002B17A03</CC>
<FD>Système nerveux pathologie; Parkinson maladie; Dyskinésie; Stimulant sérotoninergique; Stade avancé; Récepteur sérotoninergique 5-HT1A; Sérotonine; Dopamine; Lévodopa</FD>
<FG>Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie; Neurotransmetteur; Catécholamine; Mouvement involontaire; Trouble neurologique</FG>
<ED>Nervous system diseases; Parkinson disease; Dyskinesia; Serotonin agonist; Advanced stage; 5-HT1A Serotonine receptor; Serotonin; Dopamine; Levodopa</ED>
<EG>Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Neurotransmitter; Catecholamine; Involuntary movement; Neurological disorder</EG>
<SD>Sistema nervioso patología; Parkinson enfermedad; Disquinesia; Estimulante serotoninérgico; Estadio avanzado; Receptor serotoninérgico 5-HT1A; Serotonina; Dopamina; Levodopa</SD>
<LO>INIST-20953.354000132711360030</LO>
<ID>05-0444021</ID>
</server>
</inist>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Wicri/Santé/explor/MovDisordV3/Data/PascalFrancis/Corpus

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001E12 | SxmlIndent | more

HfdSelect -h $EXPLOR_AREA/Data/PascalFrancis/Corpus/biblio.hfd -nk 001E12 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Wicri/Santé
   |area=    MovDisordV3
   |flux=    PascalFrancis
   |étape=   Corpus
   |type=    RBID
   |clé=     Pascal:05-0444021
   |texte=   Effects of serotonin 5-HT1A agonist in advanced Parkinson's disease
}}

This area was generated with Dilib version V0.6.23.
Data generation: Sun Jul 3 12:29:32 2016. Site generation: Wed Feb 14 10:52:30 2024

	Movement Disorders (revue)
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Movement Disorders (revue)

Effects of serotonin 5-HT1A agonist in advanced Parkinson's disease

Effects of serotonin 5-HT1A agonist in advanced Parkinson's disease

Source :

Descripteurs français

English descriptors

Abstract

Notice en format standard (ISO 2709)

Format Inist (serveur)

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri