Administration of MPTP to the common marmoset does not alter cortical cholinergic function
Identifieur interne : 006701 ( Main/Exploration ); précédent : 006700; suivant : 006702Administration 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 [Royaume-Uni] ; S. Hunt ; R. Briggs ; P. Jenner [Royaume-Uni] ; C. D. Marsden [Royaume-Uni]Source :
- Movement Disorders [ 0885-3185 ] ; 1986.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Acetylcholine, Animals, Brain (drug effects), Callitrichinae, Caudate‐putamen, Choline O-Acetyltransferase (metabolism), Choline acetyltransferase, Dopamine, Dopamine (metabolism), Female, Frontal cortex, MPTP, Male, Marmoset, Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (metabolism), Parkinson's disease, Pyridines (adverse effects), Quinuclidinyl Benzilate (metabolism), Receptors, Cholinergic (drug effects), Tritium (diagnostic use), [3H]QNB.
- 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 acetyl‐cholinesterase. 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.
Url:
DOI: 10.1002/mds.870010207
Affiliations:
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P." last="Rose">S. P. Rose</name><affiliation wicri:level="3"><country>Royaume-Uni</country><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName><wicri:orgArea>MRC Movement Disorder Research Group, University Department of Neurology and Parkinson's Disease Society Research Centre, Institute of Psychiatry and King's College Hospital Medical School</wicri:orgArea></affiliation></author><author><name sortKey="Hunt, S" sort="Hunt, S" uniqKey="Hunt S" first="S." last="Hunt">S. Hunt</name><affiliation><wicri:noCountry code="subField">Cambridge England</wicri:noCountry></affiliation></author><author><name sortKey="Briggs, R" sort="Briggs, R" uniqKey="Briggs R" first="R." last="Briggs">R. Briggs</name><affiliation><wicri:noCountry code="subField">Southampton</wicri:noCountry></affiliation></author><author><name sortKey="Jenner, P" sort="Jenner, P" uniqKey="Jenner P" first="P." last="Jenner">P. Jenner</name><affiliation wicri:level="3"><country>Royaume-Uni</country><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName><wicri:orgArea>MRC Movement Disorder Research Group, University Department of Neurology and Parkinson's Disease Society Research Centre, Institute of Psychiatry and King's College Hospital Medical School</wicri:orgArea></affiliation></author><author><name sortKey="Marsden, C D" sort="Marsden, C D" uniqKey="Marsden C" first="C. D." last="Marsden">C. D. Marsden</name><affiliation wicri:level="3"><country>Royaume-Uni</country><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName><wicri:orgArea>MRC Movement Disorder Research Group, University Department of Neurology and Parkinson's Disease Society Research Centre, Institute of Psychiatry and King's College Hospital Medical School</wicri:orgArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</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="1986">1986</date><biblScope unit="vol">1</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="129">129</biblScope><biblScope unit="page" to="134">134</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">986CE3DCBCB6436E55757CA3387FB376AE285C13</idno><idno type="DOI">10.1002/mds.870010207</idno><idno type="ArticleID">MDS870010207</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>Acetylcholine</term><term>Animals</term><term>Brain (drug effects)</term><term>Callitrichinae</term><term>Caudate‐putamen</term><term>Choline O-Acetyltransferase (metabolism)</term><term>Choline acetyltransferase</term><term>Dopamine</term><term>Dopamine (metabolism)</term><term>Female</term><term>Frontal cortex</term><term>MPTP</term><term>Male</term><term>Marmoset</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson Disease, Secondary (metabolism)</term><term>Parkinson's disease</term><term>Pyridines (adverse effects)</term><term>Quinuclidinyl Benzilate (metabolism)</term><term>Receptors, Cholinergic (drug effects)</term><term>Tritium (diagnostic use)</term><term>[3H]QNB</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><langUsage><language ident="en">en</language></langUsage></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 acetyl‐cholinesterase. 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><affiliations><list><country><li>Royaume-Uni</li></country><region><li>Angleterre</li><li>Grand Londres</li></region><settlement><li>Londres</li></settlement></list><tree><noCountry><name sortKey="Briggs, R" sort="Briggs, R" uniqKey="Briggs R" first="R." last="Briggs">R. Briggs</name><name sortKey="Hunt, S" sort="Hunt, S" uniqKey="Hunt S" first="S." last="Hunt">S. Hunt</name><name sortKey="Petersen, M" sort="Petersen, M" uniqKey="Petersen M" first="M." last="Petersen">M. Petersen</name><name sortKey="Waters, C M" sort="Waters, C M" uniqKey="Waters C" first="C. M." last="Waters">C. M. Waters</name></noCountry><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Garvey, J" sort="Garvey, J" uniqKey="Garvey J" first="J." last="Garvey">J. Garvey</name></region><name sortKey="Jenner, P" sort="Jenner, P" uniqKey="Jenner P" first="P." last="Jenner">P. Jenner</name><name sortKey="Marsden, C D" sort="Marsden, C D" uniqKey="Marsden C" first="C. D." last="Marsden">C. D. Marsden</name><name sortKey="Rose, S P" sort="Rose, S P" uniqKey="Rose S" first="S. P." last="Rose">S. P. Rose</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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