Prevention of dyskinesia by an NMDA receptor antagonist in MPTP monkeys: effect on adenosine A2A receptors.
Identifieur interne : 001150 ( PubMed/Curation ); précédent : 001149; suivant : 001151Prevention of dyskinesia by an NMDA receptor antagonist in MPTP monkeys: effect on adenosine A2A receptors.
Auteurs : Marc Morissette [Canada] ; Mehdi Dridi ; Frédéric Calon ; Abdallah Hadj Tahar ; Leonard T. Meltzer ; Paul J. Bédard ; Thérèse Di PaoloSource :
- Synapse (New York, N.Y.) [ 0887-4476 ] ; 2006.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Animals, Anti-Dyskinesia Agents, Antiparkinson Agents (therapeutic use), Benzoxazoles (pharmacology), Denervation, Dopamine (metabolism), Dopamine Agents, Dyskinesia, Drug-Induced (prevention & control), Excitatory Amino Acid Antagonists (pharmacology), Female, Image Processing, Computer-Assisted, In Situ Hybridization, Levodopa (therapeutic use), Macaca fascicularis, Motor Activity (drug effects), Neuroprotective Agents (pharmacokinetics), Neuroprotective Agents (pharmacology), Oligonucleotide Probes, Ovariectomy, Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (prevention & control), Piperidines (pharmacology), Pyrimidines (pharmacokinetics), Pyrimidines (pharmacology), Receptor, Adenosine A2A (drug effects), Receptors, N-Methyl-D-Aspartate (antagonists & inhibitors), Triazoles (pharmacokinetics), Triazoles (pharmacology).
- MESH :
- chemical , antagonists & inhibitors : Receptors, N-Methyl-D-Aspartate.
- chemical , drug effects : Receptor, Adenosine A2A.
- chemical , metabolism : Dopamine.
- chemical , pharmacokinetics : Neuroprotective Agents, Pyrimidines, Triazoles.
- chemical , pharmacology : Benzoxazoles, Excitatory Amino Acid Antagonists, Neuroprotective Agents, Piperidines, Pyrimidines, Triazoles.
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- chemical : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Anti-Dyskinesia Agents, Dopamine Agents, Oligonucleotide Probes.
- chemically induced : Parkinson Disease, Secondary.
- drug effects : Motor Activity.
- prevention & control : Dyskinesia, Drug-Induced, Parkinson Disease, Secondary.
- Animals, Denervation, Female, Image Processing, Computer-Assisted, In Situ Hybridization, Macaca fascicularis, Ovariectomy.
Abstract
Adenosine A(2A) receptors (A(2A)R) have received increasing attention for the treatment of L-DOPA-induced dyskinesias in Parkinson disease. In the present study, A(2A)R messenger RNA (mRNA) and receptor-specific binding in the brain of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) monkeys were studied after treatment with L-DOPA and a selective NR1A/2B NMDA receptor antagonist, CI-1041. Four MPTP monkeys received L-DOPA/benserazide and all developed dyskinesias, whereas among the four MPTP monkeys who additionally received CI-1041, only one developed mild dyskinesias. Four normal monkeys and four MPTP-treated monkeys were also studied. All MPTP monkeys had similar striatal dopamine (DA) denervation. A(2A)R mRNA levels, measured by in situ hybridization, were increased in the rostral lateral caudate and putamen of saline-treated MPTP monkeys as well as in the caudal lateral and medial putamen when compared with those of controls. A(2A)R mRNA levels remained elevated in the rostral caudate and putamen of L-DOPA-treated MPTP monkeys when compared with those of controls. A(2A)R mRNA levels of L-DOPA + CI-1041-treated monkeys were at control levels and decreased in the lateral rostral caudate and caudal putamen when compared with those of L-DOPA-treated and saline-treated MPTP monkeys respectively. No change was measured in the caudal medial putamen and caudate nucleus. A(2A)Rs labeled by autoradiography with [(3)H]SCH-58261 had lower level in the L-DOPA + CI-1041-treated MPTP monkeys compared with saline- or L-DOPA-treated MPTP and control monkeys in the rostral lateral and medial caudate and the putamen. No effect of lesion or L-DOPA treatment was measured on [(3)H]SCH-58261-specific binding. These findings suggest that blockade of NMDA receptors could prevent the development of dyskinesias by altering A(2A)Rs.
DOI: 10.1002/syn.20295
PubMed: 16739115
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Meltzer</name></author><author><name sortKey="Bedard, Paul J" sort="Bedard, Paul J" uniqKey="Bedard P" first="Paul J" last="Bédard">Paul J. Bédard</name></author><author><name sortKey="Di Paolo, Therese" sort="Di Paolo, Therese" uniqKey="Di Paolo T" first="Thérèse" last="Di Paolo">Thérèse Di Paolo</name></author></analytic><series><title level="j">Synapse (New York, N.Y.)</title><idno type="ISSN">0887-4476</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>Anti-Dyskinesia Agents</term><term>Antiparkinson Agents (therapeutic use)</term><term>Benzoxazoles (pharmacology)</term><term>Denervation</term><term>Dopamine (metabolism)</term><term>Dopamine Agents</term><term>Dyskinesia, Drug-Induced (prevention & control)</term><term>Excitatory Amino Acid Antagonists (pharmacology)</term><term>Female</term><term>Image Processing, Computer-Assisted</term><term>In Situ Hybridization</term><term>Levodopa (therapeutic use)</term><term>Macaca fascicularis</term><term>Motor Activity (drug effects)</term><term>Neuroprotective Agents (pharmacokinetics)</term><term>Neuroprotective Agents (pharmacology)</term><term>Oligonucleotide Probes</term><term>Ovariectomy</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson Disease, Secondary (prevention & control)</term><term>Piperidines (pharmacology)</term><term>Pyrimidines (pharmacokinetics)</term><term>Pyrimidines (pharmacology)</term><term>Receptor, Adenosine A2A (drug effects)</term><term>Receptors, N-Methyl-D-Aspartate (antagonists & inhibitors)</term><term>Triazoles (pharmacokinetics)</term><term>Triazoles (pharmacology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Receptors, N-Methyl-D-Aspartate</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Receptor, Adenosine A2A</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacokinetics" xml:lang="en"><term>Neuroprotective Agents</term><term>Pyrimidines</term><term>Triazoles</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Benzoxazoles</term><term>Excitatory Amino Acid Antagonists</term><term>Neuroprotective Agents</term><term>Piperidines</term><term>Pyrimidines</term><term>Triazoles</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>Anti-Dyskinesia Agents</term><term>Dopamine Agents</term><term>Oligonucleotide Probes</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Motor Activity</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Dyskinesia, Drug-Induced</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Denervation</term><term>Female</term><term>Image Processing, Computer-Assisted</term><term>In Situ Hybridization</term><term>Macaca fascicularis</term><term>Ovariectomy</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Adenosine A(2A) receptors (A(2A)R) have received increasing attention for the treatment of L-DOPA-induced dyskinesias in Parkinson disease. In the present study, A(2A)R messenger RNA (mRNA) and receptor-specific binding in the brain of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) monkeys were studied after treatment with L-DOPA and a selective NR1A/2B NMDA receptor antagonist, CI-1041. Four MPTP monkeys received L-DOPA/benserazide and all developed dyskinesias, whereas among the four MPTP monkeys who additionally received CI-1041, only one developed mild dyskinesias. Four normal monkeys and four MPTP-treated monkeys were also studied. All MPTP monkeys had similar striatal dopamine (DA) denervation. A(2A)R mRNA levels, measured by in situ hybridization, were increased in the rostral lateral caudate and putamen of saline-treated MPTP monkeys as well as in the caudal lateral and medial putamen when compared with those of controls. A(2A)R mRNA levels remained elevated in the rostral caudate and putamen of L-DOPA-treated MPTP monkeys when compared with those of controls. A(2A)R mRNA levels of L-DOPA + CI-1041-treated monkeys were at control levels and decreased in the lateral rostral caudate and caudal putamen when compared with those of L-DOPA-treated and saline-treated MPTP monkeys respectively. No change was measured in the caudal medial putamen and caudate nucleus. A(2A)Rs labeled by autoradiography with [(3)H]SCH-58261 had lower level in the L-DOPA + CI-1041-treated MPTP monkeys compared with saline- or L-DOPA-treated MPTP and control monkeys in the rostral lateral and medial caudate and the putamen. No effect of lesion or L-DOPA treatment was measured on [(3)H]SCH-58261-specific binding. These findings suggest that blockade of NMDA receptors could prevent the development of dyskinesias by altering A(2A)Rs.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16739115</PMID><DateCreated><Year>2006</Year><Month>07</Month><Day>13</Day></DateCreated><DateCompleted><Year>2006</Year><Month>08</Month><Day>28</Day></DateCompleted><DateRevised><Year>2015</Year><Month>11</Month><Day>19</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0887-4476</ISSN><JournalIssue CitedMedium="Print"><Volume>60</Volume><Issue>3</Issue><PubDate><Year>2006</Year><Month>Sep</Month><Day>01</Day></PubDate></JournalIssue><Title>Synapse (New York, N.Y.)</Title><ISOAbbreviation>Synapse</ISOAbbreviation></Journal><ArticleTitle>Prevention of dyskinesia by an NMDA receptor antagonist in MPTP monkeys: effect on adenosine A2A receptors.</ArticleTitle><Pagination><MedlinePgn>239-50</MedlinePgn></Pagination><Abstract><AbstractText>Adenosine A(2A) receptors (A(2A)R) have received increasing attention for the treatment of L-DOPA-induced dyskinesias in Parkinson disease. In the present study, A(2A)R messenger RNA (mRNA) and receptor-specific binding in the brain of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) monkeys were studied after treatment with L-DOPA and a selective NR1A/2B NMDA receptor antagonist, CI-1041. Four MPTP monkeys received L-DOPA/benserazide and all developed dyskinesias, whereas among the four MPTP monkeys who additionally received CI-1041, only one developed mild dyskinesias. Four normal monkeys and four MPTP-treated monkeys were also studied. All MPTP monkeys had similar striatal dopamine (DA) denervation. A(2A)R mRNA levels, measured by in situ hybridization, were increased in the rostral lateral caudate and putamen of saline-treated MPTP monkeys as well as in the caudal lateral and medial putamen when compared with those of controls. A(2A)R mRNA levels remained elevated in the rostral caudate and putamen of L-DOPA-treated MPTP monkeys when compared with those of controls. A(2A)R mRNA levels of L-DOPA + CI-1041-treated monkeys were at control levels and decreased in the lateral rostral caudate and caudal putamen when compared with those of L-DOPA-treated and saline-treated MPTP monkeys respectively. No change was measured in the caudal medial putamen and caudate nucleus. A(2A)Rs labeled by autoradiography with [(3)H]SCH-58261 had lower level in the L-DOPA + CI-1041-treated MPTP monkeys compared with saline- or L-DOPA-treated MPTP and control monkeys in the rostral lateral and medial caudate and the putamen. No effect of lesion or L-DOPA treatment was measured on [(3)H]SCH-58261-specific binding. These findings suggest that blockade of NMDA receptors could prevent the development of dyskinesias by altering A(2A)Rs.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Morissette</LastName><ForeName>Marc</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Molecular Endocrinology and Oncology Research Centre, Laval University Medical Centre (CHUL), Quebec, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dridi</LastName><ForeName>Mehdi</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Calon</LastName><ForeName>Frédéric</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Hadj Tahar</LastName><ForeName>Abdallah</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Meltzer</LastName><ForeName>Leonard T</ForeName><Initials>LT</Initials></Author><Author ValidYN="Y"><LastName>Bédard</LastName><ForeName>Paul J</ForeName><Initials>PJ</Initials></Author><Author ValidYN="Y"><LastName>Di Paolo</LastName><ForeName>Thérèse</ForeName><Initials>T</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Synapse</MedlineTA><NlmUniqueID>8806914</NlmUniqueID><ISSNLinking>0887-4476</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C098657">5-amino-7-(2-phenylethyl)-2-(2-furyl)pyrazolo(4,3-e)-1,2,4-triazolo(1,5-c)pyrimidine</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018726">Anti-Dyskinesia Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson 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A2A</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016194">Receptors, N-Methyl-D-Aspartate</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014230">Triazoles</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical><Chemical><RegistryNumber>5K3N2D15WW</RegistryNumber><NameOfSubstance UI="C481484">besonprodil</NameOfSubstance></Chemical><Chemical><RegistryNumber>9P21XSP91P</RegistryNumber><NameOfSubstance UI="D015632">1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D015632" MajorTopicYN="Y">1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018726" MajorTopicYN="Y">Anti-Dyskinesia Agents</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000978" MajorTopicYN="N">Antiparkinson Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001583" MajorTopicYN="N">Benzoxazoles</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003714" MajorTopicYN="N">Denervation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004298" MajorTopicYN="N">Dopamine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015259" MajorTopicYN="Y">Dopamine Agents</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004409" MajorTopicYN="N">Dyskinesia, Drug-Induced</DescriptorName><QualifierName UI="Q000517" MajorTopicYN="Y">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018691" MajorTopicYN="N">Excitatory Amino Acid Antagonists</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007091" MajorTopicYN="N">Image Processing, Computer-Assisted</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017403" MajorTopicYN="N">In Situ Hybridization</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007980" MajorTopicYN="N">Levodopa</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008252" MajorTopicYN="N">Macaca fascicularis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009043" MajorTopicYN="N">Motor Activity</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018696" MajorTopicYN="N">Neuroprotective Agents</DescriptorName><QualifierName UI="Q000493" MajorTopicYN="N">pharmacokinetics</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015345" MajorTopicYN="N">Oligonucleotide Probes</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010052" MajorTopicYN="N">Ovariectomy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010302" MajorTopicYN="N">Parkinson Disease, Secondary</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="Y">chemically induced</QualifierName><QualifierName UI="Q000517" MajorTopicYN="Y">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010880" MajorTopicYN="N">Piperidines</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011743" MajorTopicYN="N">Pyrimidines</DescriptorName><QualifierName UI="Q000493" MajorTopicYN="N">pharmacokinetics</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D043705" MajorTopicYN="N">Receptor, Adenosine A2A</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016194" MajorTopicYN="N">Receptors, N-Methyl-D-Aspartate</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="Y">antagonists & inhibitors</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014230" MajorTopicYN="N">Triazoles</DescriptorName><QualifierName UI="Q000493" MajorTopicYN="N">pharmacokinetics</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2006</Year><Month>6</Month><Day>2</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2006</Year><Month>8</Month><Day>29</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2006</Year><Month>6</Month><Day>2</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">16739115</ArticleId><ArticleId IdType="doi">10.1002/syn.20295</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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