D1 receptor agonist improves sleep-wake parameters in experimental parkinsonism
Identifieur interne : 000249 ( Hal/Corpus ); précédent : 000248; suivant : 000250D1 receptor agonist improves sleep-wake parameters in experimental parkinsonism
Auteurs : Carole Hyacinthe ; Quentin Barraud ; François Tison ; Erwan Bezard ; Imad GhorayebSource :
- Neurobiology of Disease [ 0969-9961 ] ; 2014-03-03.
Abstract
Both excessive daytime sleepiness (EDS) and rapid eye movement (REM) sleep deregulation are part of Parkinson's disease (PD) non-motor symptoms and may complicate dopamine replacement therapy. We report here that dopamine agonists act differentially on sleep architecture in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine macaque monkey. Continuous sleep and wake electroencephalographic monitoring revealed no effect of the selective dopamine D2 receptor agonist quinpirole on EDS, whereas the selective dopamine D1 receptor agonist SKF38393 efficiently alleviated EDS and restored REM sleep to baseline values. The present results question the relevance of abandoning D1 receptor agonist treatment in PD as it might actually improve sleep-related disorders.
Url:
DOI: 10.1016/j.nbd.2013.10.029
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<front><div type="abstract" xml:lang="en">Both excessive daytime sleepiness (EDS) and rapid eye movement (REM) sleep deregulation are part of Parkinson's disease (PD) non-motor symptoms and may complicate dopamine replacement therapy. We report here that dopamine agonists act differentially on sleep architecture in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine macaque monkey. Continuous sleep and wake electroencephalographic monitoring revealed no effect of the selective dopamine D2 receptor agonist quinpirole on EDS, whereas the selective dopamine D1 receptor agonist SKF38393 efficiently alleviated EDS and restored REM sleep to baseline values. The present results question the relevance of abandoning D1 receptor agonist treatment in PD as it might actually improve sleep-related disorders.</div>
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<idno type="halId">hal-01048645</idno>
<idno type="halUri">https://hal.archives-ouvertes.fr/hal-01048645</idno>
<idno type="halBibtex">hyacinthe:hal-01048645</idno>
<idno type="halRefHtml">Neurobiology of Disease, Elsevier, 2014, 63, pp.20. <10.1016/j.nbd.2013.10.029></idno>
<idno type="halRef">Neurobiology of Disease, Elsevier, 2014, 63, pp.20. <10.1016/j.nbd.2013.10.029></idno>
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</seriesStmt>
<notesStmt> <note type="audience" n="2">International</note>
<note type="popular" n="0">No</note>
<note type="peer" n="1">Yes</note>
</notesStmt>
<sourceDesc> <biblStruct> <analytic> <title xml:lang="en">D1 receptor agonist improves sleep-wake parameters in experimental parkinsonism</title>
<author role="aut"> <persName> <forename type="first">Carole</forename>
<surname>Hyacinthe</surname>
</persName>
<idno type="halauthorid">600721</idno>
<affiliation ref="#struct-139693"></affiliation>
<affiliation ref="#struct-244085"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Quentin</forename>
<surname>Barraud</surname>
</persName>
<idno type="halauthorid">1059419</idno>
<affiliation ref="#struct-244085"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">François</forename>
<surname>Tison</surname>
</persName>
<idno type="halauthorid">224383</idno>
<affiliation ref="#struct-244085"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Erwan</forename>
<surname>Bezard</surname>
</persName>
<email type="md5">b0deb6c343e8d1ae022cfd4a58cecc43</email>
<email type="domain">u-bordeaux2.fr</email>
<idno type="halauthorid">506531</idno>
<affiliation ref="#struct-244085"></affiliation>
</author>
<author role="crp"> <persName> <forename type="first">Imad</forename>
<surname>Ghorayeb</surname>
</persName>
<email type="md5">0e29adf391ab4782c9207181c2c3022a</email>
<email type="domain">u-bordeaux2.fr</email>
<idno type="halauthorid">1059420</idno>
<affiliation ref="#struct-244085"></affiliation>
</author>
</analytic>
<monogr> <idno type="halJournalId" status="VALID">13277</idno>
<idno type="issn">0969-9961</idno>
<idno type="eissn">1095-953X</idno>
<title level="j">Neurobiology of Disease</title>
<imprint> <publisher>Elsevier</publisher>
<biblScope unit="volume">63</biblScope>
<biblScope unit="pp">20</biblScope>
<date type="datePub">2014-03-03</date>
</imprint>
</monogr>
<idno type="doi">10.1016/j.nbd.2013.10.029</idno>
<idno type="pubmed">24211719</idno>
</biblStruct>
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<profileDesc> <langUsage> <language ident="en">English</language>
</langUsage>
<textClass> <classCode scheme="halDomain" n="scco.neur">Cognitive science/Neuroscience</classCode>
<classCode scheme="halTypology" n="ART">Journal articles</classCode>
</textClass>
<abstract xml:lang="en">Both excessive daytime sleepiness (EDS) and rapid eye movement (REM) sleep deregulation are part of Parkinson's disease (PD) non-motor symptoms and may complicate dopamine replacement therapy. We report here that dopamine agonists act differentially on sleep architecture in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine macaque monkey. Continuous sleep and wake electroencephalographic monitoring revealed no effect of the selective dopamine D2 receptor agonist quinpirole on EDS, whereas the selective dopamine D1 receptor agonist SKF38393 efficiently alleviated EDS and restored REM sleep to baseline values. The present results question the relevance of abandoning D1 receptor agonist treatment in PD as it might actually improve sleep-related disorders.</abstract>
</profileDesc>
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