Effects of serotonin 5‐HT1A agonist in advanced Parkinson's disease
Identifieur interne : 002407 ( Istex/Corpus ); précédent : 002406; suivant : 002408Effects 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. ChaseSource :
- Movement Disorders [ 0885-3185 ] ; 2005-08.
English descriptors
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. © 2005 Movement Disorder Society
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DOI: 10.1002/mds.20370
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<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. © 2005 Movement Disorder Society</div>
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<creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>William</givenNames>
<familyName>Bara‐Jimenez</familyName>
<degrees>MD</degrees>
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<contactDetails><email>Baraw@ninds.nih.gov</email>
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<creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Michael J.</givenNames>
<familyName>Morris</familyName>
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<creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Tzvetelina</givenNames>
<familyName>Dimitrova</familyName>
<degrees>MD</degrees>
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<creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Abdullah</givenNames>
<familyName>Sherzai</familyName>
<degrees>MD</degrees>
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<creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Maral M.</givenNames>
<familyName>Mouradian</familyName>
<degrees>MD</degrees>
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<creator xml:id="au7" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Thomas N.</givenNames>
<familyName>Chase</familyName>
<degrees>MD</degrees>
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<keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">5‐HT1A receptor</keyword>
<keyword xml:id="kwd2">serotonin</keyword>
<keyword xml:id="kwd3">dopamine</keyword>
<keyword xml:id="kwd4">Parkinson's disease</keyword>
<keyword xml:id="kwd5">dyskinesias, levodopa</keyword>
<keyword xml:id="kwd6">striatum</keyword>
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<p>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 (<i>P</i>
≤ 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. © 2005 Movement Disorder Society</p>
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<!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Effects of serotonin 5‐HT1A agonist in advanced Parkinson's disease</title>
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<titleInfo type="abbreviated" lang="en"><title>5‐HT1A Agonist Effects in Parkinson's Disease</title>
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<titleInfo type="alternative" contentType="CDATA" lang="en"><title>Effects of serotonin 5‐HT1A agonist in advanced Parkinson's disease</title>
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<name type="personal"><namePart type="given">William</namePart>
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<namePart type="termsOfAddress">MD</namePart>
<affiliation>Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA</affiliation>
<description>Correspondence: Bldg. 10, Rm. 5C103, National Institutes of Health, Bethesda, MD 20892</description>
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<name type="personal"><namePart type="given">Michael J.</namePart>
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<name type="personal"><namePart type="given">Tzvetelina</namePart>
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<affiliation>Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA</affiliation>
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<name type="personal"><namePart type="given">Abdullah</namePart>
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<name type="personal"><namePart type="given">Maral M.</namePart>
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<role><roleTerm type="text">author</roleTerm>
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<name type="personal"><namePart type="given">Thomas N.</namePart>
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<abstract 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. © 2005 Movement Disorder Society</abstract>
<subject lang="en"><genre>Keywords</genre>
<topic>5‐HT1A receptor</topic>
<topic>serotonin</topic>
<topic>dopamine</topic>
<topic>Parkinson's disease</topic>
<topic>dyskinesias, levodopa</topic>
<topic>striatum</topic>
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<relatedItem type="host"><titleInfo><title>Movement Disorders</title>
<subTitle>Official Journal of the Movement Disorder Society</subTitle>
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<identifier type="ISSN">0885-3185</identifier>
<identifier type="eISSN">1531-8257</identifier>
<identifier type="DOI">10.1002/(ISSN)1531-8257</identifier>
<identifier type="PublisherID">MDS</identifier>
<part><date>2005</date>
<detail type="volume"><caption>vol.</caption>
<number>20</number>
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<detail type="issue"><caption>no.</caption>
<number>8</number>
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<accessCondition type="use and reproduction" contentType="copyright">Copyright © 2005 Movement Disorder Society</accessCondition>
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