Administration of MPTP to the common marmoset does not alter cortical cholinergic function.
Identifieur interne : 005124 ( PubMed/Curation ); précédent : 005123; suivant : 005125Administration of MPTP to the common marmoset does not alter cortical cholinergic function.
Auteurs : J. Garvey [Royaume-Uni] ; M. Petersen ; C M Waters ; S P Rose ; S. Hunt ; R. Briggs ; P. Jenner ; C D MarsdenSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1986.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Animals, Brain (drug effects), Callitrichinae, Choline O-Acetyltransferase (metabolism), Dopamine (metabolism), Female, Male, Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (metabolism), Pyridines (adverse effects), Quinuclidinyl Benzilate (metabolism), Receptors, Cholinergic (drug effects), Tritium (diagnostic use).
- MESH :
- chemical , adverse effects : Pyridines.
- chemical , diagnostic use : Tritium.
- chemical , drug effects : Receptors, Cholinergic.
- chemical , metabolism : Choline O-Acetyltransferase, Dopamine, Quinuclidinyl Benzilate.
- chemical : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine.
- chemically induced : Parkinson Disease, Secondary.
- drug effects : Brain.
- metabolism : Parkinson Disease, Secondary.
- Animals, Callitrichinae, Female, Male.
Abstract
The administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to common marmosets induced persistent motor deficits and decreased concentrations of dopamine, homovanillic acid, and 3,4-dihydroxy-phenylacetic acid (DOPAC) and [3H]dopamine uptake in the caudate-putamen. There was an 80% reduction in tyrosine hydroxylase immunoreactive cells in substantia nigra. At 10 days following the start of MPTP administration, the activity of choline acetyltransferase in the thalamus and frontal cortex was unchanged compared with control animals. Similarly, specific [3H]QNB binding was unaltered. At 4-6 weeks following the start of MPTP treatment, choline acetyltransferase activity and [3H]QNB binding in the frontal cortex and thalamus remained unaffected. There was no evidence for cell loss in the nucleus basalis of Meynert or alteration in the intensity of staining for acetylcholinesterase. MPTP treatment of the common marmoset produces a nigrostriatal lesion. In contrast, MPTP did not alter cortical cholinergic function and was not neurotoxic to the cholinergic cells in the nucleus basalis of Meynert.
DOI: 10.1002/mds.870010207
PubMed: 3143064
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Petersen</name></author><author><name sortKey="Waters, C M" sort="Waters, C M" uniqKey="Waters C" first="C M" last="Waters">C M Waters</name></author><author><name sortKey="Rose, S P" sort="Rose, S P" uniqKey="Rose S" first="S P" last="Rose">S P Rose</name></author><author><name sortKey="Hunt, S" sort="Hunt, S" uniqKey="Hunt S" first="S" last="Hunt">S. Hunt</name></author><author><name sortKey="Briggs, R" sort="Briggs, R" uniqKey="Briggs R" first="R" last="Briggs">R. Briggs</name></author><author><name sortKey="Jenner, P" sort="Jenner, P" uniqKey="Jenner P" first="P" last="Jenner">P. Jenner</name></author><author><name sortKey="Marsden, C D" sort="Marsden, C D" uniqKey="Marsden C" first="C D" last="Marsden">C D Marsden</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1986">1986</date><idno type="RBID">pubmed:3143064</idno><idno type="pmid">3143064</idno><idno type="doi">10.1002/mds.870010207</idno><idno type="wicri:Area/PubMed/Corpus">005124</idno><idno type="wicri:Area/PubMed/Curation">005124</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Administration of MPTP to the common marmoset does not alter cortical cholinergic function.</title><author><name sortKey="Garvey, J" sort="Garvey, J" uniqKey="Garvey J" first="J" last="Garvey">J. Garvey</name><affiliation wicri:level="2"><nlm:affiliation>University Department of Neurology, Institute of Psychiatry, London, England.</nlm:affiliation><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>University Department of Neurology, Institute of Psychiatry, London</wicri:cityArea></affiliation></author><author><name sortKey="Petersen, M" sort="Petersen, M" uniqKey="Petersen M" first="M" last="Petersen">M. Petersen</name></author><author><name sortKey="Waters, C M" sort="Waters, C M" uniqKey="Waters C" first="C M" last="Waters">C M Waters</name></author><author><name sortKey="Rose, S P" sort="Rose, S P" uniqKey="Rose S" first="S P" last="Rose">S P Rose</name></author><author><name sortKey="Hunt, S" sort="Hunt, S" uniqKey="Hunt S" first="S" last="Hunt">S. Hunt</name></author><author><name sortKey="Briggs, R" sort="Briggs, R" uniqKey="Briggs R" first="R" last="Briggs">R. Briggs</name></author><author><name sortKey="Jenner, P" sort="Jenner, P" uniqKey="Jenner P" first="P" last="Jenner">P. Jenner</name></author><author><name sortKey="Marsden, C D" sort="Marsden, C D" uniqKey="Marsden C" first="C D" last="Marsden">C D Marsden</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="1986" type="published">1986</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>Brain (drug effects)</term><term>Callitrichinae</term><term>Choline O-Acetyltransferase (metabolism)</term><term>Dopamine (metabolism)</term><term>Female</term><term>Male</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson Disease, Secondary (metabolism)</term><term>Pyridines (adverse effects)</term><term>Quinuclidinyl Benzilate (metabolism)</term><term>Receptors, Cholinergic (drug effects)</term><term>Tritium (diagnostic use)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Pyridines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="diagnostic use" xml:lang="en"><term>Tritium</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Receptors, Cholinergic</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Choline O-Acetyltransferase</term><term>Dopamine</term><term>Quinuclidinyl Benzilate</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>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Brain</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Callitrichinae</term><term>Female</term><term>Male</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to common marmosets induced persistent motor deficits and decreased concentrations of dopamine, homovanillic acid, and 3,4-dihydroxy-phenylacetic acid (DOPAC) and [3H]dopamine uptake in the caudate-putamen. There was an 80% reduction in tyrosine hydroxylase immunoreactive cells in substantia nigra. At 10 days following the start of MPTP administration, the activity of choline acetyltransferase in the thalamus and frontal cortex was unchanged compared with control animals. Similarly, specific [3H]QNB binding was unaltered. At 4-6 weeks following the start of MPTP treatment, choline acetyltransferase activity and [3H]QNB binding in the frontal cortex and thalamus remained unaffected. There was no evidence for cell loss in the nucleus basalis of Meynert or alteration in the intensity of staining for acetylcholinesterase. MPTP treatment of the common marmoset produces a nigrostriatal lesion. In contrast, MPTP did not alter cortical cholinergic function and was not neurotoxic to the cholinergic cells in the nucleus basalis of Meynert.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">3143064</PMID><DateCreated><Year>1989</Year><Month>01</Month><Day>10</Day></DateCreated><DateCompleted><Year>1989</Year><Month>01</Month><Day>10</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>1</Volume><Issue>2</Issue><PubDate><Year>1986</Year></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Administration of MPTP to the common marmoset does not alter cortical cholinergic function.</ArticleTitle><Pagination><MedlinePgn>129-34</MedlinePgn></Pagination><Abstract><AbstractText>The administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to common marmosets induced persistent motor deficits and decreased concentrations of dopamine, homovanillic acid, and 3,4-dihydroxy-phenylacetic acid (DOPAC) and [3H]dopamine uptake in the caudate-putamen. There was an 80% reduction in tyrosine hydroxylase immunoreactive cells in substantia nigra. At 10 days following the start of MPTP administration, the activity of choline acetyltransferase in the thalamus and frontal cortex was unchanged compared with control animals. Similarly, specific [3H]QNB binding was unaltered. At 4-6 weeks following the start of MPTP treatment, choline acetyltransferase activity and [3H]QNB binding in the frontal cortex and thalamus remained unaffected. There was no evidence for cell loss in the nucleus basalis of Meynert or alteration in the intensity of staining for acetylcholinesterase. MPTP treatment of the common marmoset produces a nigrostriatal lesion. In contrast, MPTP did not alter cortical cholinergic function and was not neurotoxic to the cholinergic cells in the nucleus basalis of Meynert.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Garvey</LastName><ForeName>J</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>University Department of Neurology, Institute of Psychiatry, London, England.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Petersen</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Waters</LastName><ForeName>C M</ForeName><Initials>CM</Initials></Author><Author ValidYN="Y"><LastName>Rose</LastName><ForeName>S P</ForeName><Initials>SP</Initials></Author><Author ValidYN="Y"><LastName>Hunt</LastName><ForeName>S</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Briggs</LastName><ForeName>R</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Jenner</LastName><ForeName>P</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Marsden</LastName><ForeName>C D</ForeName><Initials>CD</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>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011725">Pyridines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011950">Receptors, Cholinergic</NameOfSubstance></Chemical><Chemical><RegistryNumber>10028-17-8</RegistryNumber><NameOfSubstance UI="D014316">Tritium</NameOfSubstance></Chemical><Chemical><RegistryNumber>6581-06-2</RegistryNumber><NameOfSubstance UI="D011813">Quinuclidinyl Benzilate</NameOfSubstance></Chemical><Chemical><RegistryNumber>9P21XSP91P</RegistryNumber><NameOfSubstance UI="D015632">1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.3.1.6</RegistryNumber><NameOfSubstance UI="D002795">Choline O-Acetyltransferase</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D015632">1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000818">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001921">Brain</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000187">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002143">Callitrichinae</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002795">Choline O-Acetyltransferase</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004298">Dopamine</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010302">Parkinson Disease, Secondary</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000139">chemically induced</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011725">Pyridines</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000009">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011813">Quinuclidinyl Benzilate</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011950">Receptors, Cholinergic</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000187">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D014316">Tritium</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000176">diagnostic use</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1986</Year><Month>1</Month><Day>1</Day></PubMedPubDate><PubMedPubDate 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