Administration of MPTP to the common marmoset does not alter cortical cholinergic function.
Identifieur interne : 005124 ( PubMed/Corpus ); précédent : 005123; suivant : 005125Administration of MPTP to the common marmoset does not alter cortical cholinergic function.
Auteurs : J. Garvey ; 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
Links to Exploration step
pubmed:3143064Le document en format XML
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<author><name sortKey="Garvey, J" sort="Garvey, J" uniqKey="Garvey J" first="J" last="Garvey">J. Garvey</name>
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<author><name sortKey="Waters, C M" sort="Waters, C M" uniqKey="Waters C" first="C M" last="Waters">C M Waters</name>
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<author><name sortKey="Rose, S P" sort="Rose, S P" uniqKey="Rose S" first="S P" last="Rose">S P Rose</name>
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<author><name sortKey="Hunt, S" sort="Hunt, S" uniqKey="Hunt S" first="S" last="Hunt">S. Hunt</name>
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<author><name sortKey="Briggs, R" sort="Briggs, R" uniqKey="Briggs R" first="R" last="Briggs">R. Briggs</name>
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<author><name sortKey="Jenner, P" sort="Jenner, P" uniqKey="Jenner P" first="P" last="Jenner">P. Jenner</name>
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<author><name sortKey="Marsden, C D" sort="Marsden, C D" uniqKey="Marsden C" first="C D" last="Marsden">C D Marsden</name>
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<term>Callitrichinae</term>
<term>Choline O-Acetyltransferase (metabolism)</term>
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<term>Parkinson Disease, Secondary (metabolism)</term>
<term>Pyridines (adverse effects)</term>
<term>Quinuclidinyl Benzilate (metabolism)</term>
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<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Choline O-Acetyltransferase</term>
<term>Dopamine</term>
<term>Quinuclidinyl Benzilate</term>
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<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>
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<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>
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