Histamine H3 receptor agonists reduce L‐dopa–induced chorea, but not dystonia, in the MPTP‐lesioned nonhuman primate model of Parkinson's disease
Identifieur interne : 004716 ( Main/Merge ); précédent : 004715; suivant : 004717Histamine H3 receptor agonists reduce L‐dopa–induced chorea, but not dystonia, in the MPTP‐lesioned nonhuman primate model of Parkinson's disease
Auteurs : Jordi Gomez-Ramirez [Canada] ; Tom H. Johnston [Canada] ; Naomi P. Visanji [Canada] ; Susan H. Fox [Canada] ; Jonathan M. Brotchie [Canada]Source :
- Movement Disorders [ 0885-3185 ] ; 2006-06-06.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Animals, Callithrix, Chorea (chemically induced), Chorea (prevention & control), Disease Models, Animal, Female, Histamine Agonists (pharmacology), Levodopa (adverse effects), L‐dopa–induced dyskinesia, MPTP‐lesioned marmoset, Parkinson Disease (drug therapy), Parkinson Disease (physiopathology), Parkinson's disease, Receptors, Histamine H3 (physiology), histamine H3 receptor agonist.
- MESH :
- chemical , adverse effects : Levodopa.
- chemical , pharmacology : Histamine Agonists.
- chemical , physiology : Receptors, Histamine H3.
- chemical : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine.
- chemically induced : Chorea.
- drug therapy : Parkinson Disease.
- physiopathology : Parkinson Disease.
- prevention & control : Chorea.
- Animals, Callithrix, Disease Models, Animal, Female.
Abstract
L‐dopa–induced dyskinesia (LID) remains a major complication of the treatment of Parkinson's disease. The neural mechanisms underlying LID are thought to involve overactivity of striatal glutamatergic neurotransmission, with resultant underactivation of the output regions of the basal ganglia. Histamine H3 heteroreceptors can reduce glutamate and γ‐aminobutyric acid (GABA) transmission in the striatum and substantia nigra reticulata, respectively. Thus, we tested whether the histamine H3 receptor agonists immepip and imetit can alleviate LID in the MPTP‐lesioned marmoset model of Parkinson's disease. Coadministration of immepip (1 mg/kg) with L‐dopa (15 mg/kg) was associated with significantly less total dyskinesia than L‐dopa alone. When dyskinesia was separately rated as chorea and dystonia, coadministration of L‐dopa with either immepip or imetit (both 10 mg/kg) significantly reduced chorea but had no effect on dystonia. The antidyskinetic actions of the H3 agonists were not accompanied by alteration of the antiparkinsonian actions of L‐dopa. However, immepip (10 mg/kg), when administered as monotherapy, significantly increased parkinsonian disability compared to vehicle. Overall, the results obtained in this study suggest that histamine H3 receptors may be involved in the neural mechanisms underlying L‐dopa–induced dyskinesia in Parkinson's disease. © 2006 Movement Disorder Society
Url:
DOI: 10.1002/mds.20828
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ISTEX:855A426357D319975E05A256C1724337E8331864Le document en format XML
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Fox</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Movement Disorders Clinic, Division of Neurology, Toronto Western Hospital, Toronto, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author><author><name sortKey="Brotchie, Jonathan M" sort="Brotchie, Jonathan M" uniqKey="Brotchie J" first="Jonathan M." last="Brotchie">Jonathan M. Brotchie</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Toronto Western Research Institute, Toronto Western Hospital, University Health Network, Toronto, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2006-06-06">2006-06-06</date><biblScope unit="vol">21</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="839">839</biblScope><biblScope unit="page" to="846">846</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">855A426357D319975E05A256C1724337E8331864</idno><idno type="DOI">10.1002/mds.20828</idno><idno type="ArticleID">MDS20828</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>Animals</term><term>Callithrix</term><term>Chorea (chemically induced)</term><term>Chorea (prevention & control)</term><term>Disease Models, Animal</term><term>Female</term><term>Histamine Agonists (pharmacology)</term><term>Levodopa (adverse effects)</term><term>L‐dopa–induced dyskinesia</term><term>MPTP‐lesioned marmoset</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson's disease</term><term>Receptors, Histamine H3 (physiology)</term><term>histamine H3 receptor agonist</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Histamine Agonists</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Receptors, Histamine H3</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Chorea</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Chorea</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Callithrix</term><term>Disease Models, Animal</term><term>Female</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">L‐dopa–induced dyskinesia (LID) remains a major complication of the treatment of Parkinson's disease. 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However, immepip (10 mg/kg), when administered as monotherapy, significantly increased parkinsonian disability compared to vehicle. Overall, the results obtained in this study suggest that histamine H3 receptors may be involved in the neural mechanisms underlying L‐dopa–induced dyskinesia in Parkinson's disease. © 2006 Movement Disorder Society</div></front></TEI><double doi="10.1002/mds.20828"><ISTEX><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Histamine H3 receptor agonists reduce L‐dopa–induced chorea, but not dystonia, in the MPTP‐lesioned nonhuman primate model of Parkinson's disease</title><author><name sortKey="Gomez Amirez, Jordi" sort="Gomez Amirez, Jordi" uniqKey="Gomez Amirez J" first="Jordi" last="Gomez-Ramirez">Jordi Gomez-Ramirez</name></author><author><name sortKey="Johnston, Tom H" sort="Johnston, Tom H" uniqKey="Johnston T" first="Tom H." last="Johnston">Tom H. Johnston</name></author><author><name sortKey="Visanji, Naomi P" sort="Visanji, Naomi P" uniqKey="Visanji N" first="Naomi P." last="Visanji">Naomi P. Visanji</name></author><author><name sortKey="Fox, Susan H" sort="Fox, Susan H" uniqKey="Fox S" first="Susan H." last="Fox">Susan H. Fox</name></author><author><name sortKey="Brotchie, Jonathan M" sort="Brotchie, Jonathan M" uniqKey="Brotchie J" first="Jonathan M." last="Brotchie">Jonathan M. 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Johnston</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Toronto Western Research Institute, Toronto Western Hospital, University Health Network, Toronto, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author><author><name sortKey="Visanji, Naomi P" sort="Visanji, Naomi P" uniqKey="Visanji N" first="Naomi P." last="Visanji">Naomi P. Visanji</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Toronto Western Research Institute, Toronto Western Hospital, University Health Network, Toronto, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author><author><name sortKey="Fox, Susan H" sort="Fox, Susan H" uniqKey="Fox S" first="Susan H." last="Fox">Susan H. Fox</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Movement Disorders Clinic, Division of Neurology, Toronto Western Hospital, Toronto, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author><author><name sortKey="Brotchie, Jonathan M" sort="Brotchie, Jonathan M" uniqKey="Brotchie J" first="Jonathan M." last="Brotchie">Jonathan M. Brotchie</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Toronto Western Research Institute, Toronto Western Hospital, University Health Network, Toronto, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2006-06-06">2006-06-06</date><biblScope unit="vol">21</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="839">839</biblScope><biblScope unit="page" to="846">846</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">855A426357D319975E05A256C1724337E8331864</idno><idno type="DOI">10.1002/mds.20828</idno><idno type="ArticleID">MDS20828</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>L‐dopa–induced dyskinesia</term><term>MPTP‐lesioned marmoset</term><term>Parkinson's disease</term><term>histamine H3 receptor agonist</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">L‐dopa–induced dyskinesia (LID) remains a major complication of the treatment of Parkinson's disease. The neural mechanisms underlying LID are thought to involve overactivity of striatal glutamatergic neurotransmission, with resultant underactivation of the output regions of the basal ganglia. Histamine H3 heteroreceptors can reduce glutamate and γ‐aminobutyric acid (GABA) transmission in the striatum and substantia nigra reticulata, respectively. Thus, we tested whether the histamine H3 receptor agonists immepip and imetit can alleviate LID in the MPTP‐lesioned marmoset model of Parkinson's disease. Coadministration of immepip (1 mg/kg) with L‐dopa (15 mg/kg) was associated with significantly less total dyskinesia than L‐dopa alone. When dyskinesia was separately rated as chorea and dystonia, coadministration of L‐dopa with either immepip or imetit (both 10 mg/kg) significantly reduced chorea but had no effect on dystonia. The antidyskinetic actions of the H3 agonists were not accompanied by alteration of the antiparkinsonian actions of L‐dopa. However, immepip (10 mg/kg), when administered as monotherapy, significantly increased parkinsonian disability compared to vehicle. Overall, the results obtained in this study suggest that histamine H3 receptors may be involved in the neural mechanisms underlying L‐dopa–induced dyskinesia in Parkinson's disease. © 2006 Movement Disorder Society</div></front></TEI></ISTEX><PubMed><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Histamine H3 receptor agonists reduce L-dopa-induced chorea, but not dystonia, in the MPTP-lesioned nonhuman primate model of Parkinson's disease.</title><author><name sortKey="Gomez Ramirez, Jordi" sort="Gomez Ramirez, Jordi" uniqKey="Gomez Ramirez J" first="Jordi" last="Gomez-Ramirez">Jordi Gomez-Ramirez</name><affiliation wicri:level="1"><nlm:affiliation>Toronto Western Research Institute, Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Toronto Western Research Institute, Toronto Western Hospital, University Health Network, Toronto, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author><author><name sortKey="Johnston, Tom H" sort="Johnston, Tom H" uniqKey="Johnston T" first="Tom H" last="Johnston">Tom H. Johnston</name></author><author><name sortKey="Visanji, Naomi P" sort="Visanji, Naomi P" uniqKey="Visanji N" first="Naomi P" last="Visanji">Naomi P. Visanji</name></author><author><name sortKey="Fox, Susan H" sort="Fox, Susan H" uniqKey="Fox S" first="Susan H" last="Fox">Susan H. Fox</name></author><author><name sortKey="Brotchie, Jonathan M" sort="Brotchie, Jonathan M" uniqKey="Brotchie J" first="Jonathan M" last="Brotchie">Jonathan M. Brotchie</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2006">2006</date><idno type="doi">10.1002/mds.20828</idno><idno type="RBID">pubmed:16532454</idno><idno type="pmid">16532454</idno><idno type="wicri:Area/PubMed/Corpus">002D40</idno><idno type="wicri:Area/PubMed/Curation">002D40</idno><idno type="wicri:Area/PubMed/Checkpoint">002C94</idno><idno type="wicri:Area/Ncbi/Merge">001591</idno><idno type="wicri:Area/Ncbi/Curation">001591</idno><idno type="wicri:Area/Ncbi/Checkpoint">001591</idno><idno type="wicri:doubleKey">0885-3185:2006:Gomez Ramirez J:histamine:h:receptor</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Histamine H3 receptor agonists reduce L-dopa-induced chorea, but not dystonia, in the MPTP-lesioned nonhuman primate model of Parkinson's disease.</title><author><name sortKey="Gomez Ramirez, Jordi" sort="Gomez Ramirez, Jordi" uniqKey="Gomez Ramirez J" first="Jordi" last="Gomez-Ramirez">Jordi Gomez-Ramirez</name><affiliation wicri:level="1"><nlm:affiliation>Toronto Western Research Institute, Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Toronto Western Research Institute, Toronto Western Hospital, University Health Network, Toronto, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author><author><name sortKey="Johnston, Tom H" sort="Johnston, Tom H" uniqKey="Johnston T" first="Tom H" last="Johnston">Tom H. Johnston</name></author><author><name sortKey="Visanji, Naomi P" sort="Visanji, Naomi P" uniqKey="Visanji N" first="Naomi P" last="Visanji">Naomi P. Visanji</name></author><author><name sortKey="Fox, Susan H" sort="Fox, Susan H" uniqKey="Fox S" first="Susan H" last="Fox">Susan H. Fox</name></author><author><name sortKey="Brotchie, Jonathan M" sort="Brotchie, Jonathan M" uniqKey="Brotchie J" first="Jonathan M" last="Brotchie">Jonathan M. Brotchie</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2006" type="published">2006</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>Animals</term><term>Callithrix</term><term>Chorea (chemically induced)</term><term>Chorea (prevention & control)</term><term>Disease Models, Animal</term><term>Female</term><term>Histamine Agonists (pharmacology)</term><term>Levodopa (adverse effects)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (physiopathology)</term><term>Receptors, Histamine H3 (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Histamine Agonists</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Receptors, Histamine H3</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Chorea</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Chorea</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Callithrix</term><term>Disease Models, Animal</term><term>Female</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">L-dopa-induced dyskinesia (LID) remains a major complication of the treatment of Parkinson's disease. The neural mechanisms underlying LID are thought to involve overactivity of striatal glutamatergic neurotransmission, with resultant underactivation of the output regions of the basal ganglia. Histamine H3 heteroreceptors can reduce glutamate and gamma-aminobutyric acid (GABA) transmission in the striatum and substantia nigra reticulata, respectively. Thus, we tested whether the histamine H3 receptor agonists immepip and imetit can alleviate LID in the MPTP-lesioned marmoset model of Parkinson's disease. Coadministration of immepip (1 mg/kg) with L-dopa (15 mg/kg) was associated with significantly less total dyskinesia than L-dopa alone. When dyskinesia was separately rated as chorea and dystonia, coadministration of L-dopa with either immepip or imetit (both 10 mg/kg) significantly reduced chorea but had no effect on dystonia. The antidyskinetic actions of the H3 agonists were not accompanied by alteration of the antiparkinsonian actions of L-dopa. However, immepip (10 mg/kg), when administered as monotherapy, significantly increased parkinsonian disability compared to vehicle. Overall, the results obtained in this study suggest that histamine H3 receptors may be involved in the neural mechanisms underlying L-dopa-induced dyskinesia in Parkinson's disease.</div></front></TEI></PubMed></double></record>Pour manipuler ce document sous Unix (Dilib)
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