Choline acetyltransferase activity and [3H]vesamicol binding in the temporal cortex of patients with Alzheimer's disease, Parkinson's disease, and rats with basal forebrain lesions.
Identifieur interne : 001829 ( PubMed/Corpus ); précédent : 001828; suivant : 001830Choline acetyltransferase activity and [3H]vesamicol binding in the temporal cortex of patients with Alzheimer's disease, Parkinson's disease, and rats with basal forebrain lesions.
Auteurs : M. Ruberg ; W. Mayo ; A. Brice ; C. Duyckaerts ; J J Hauw ; H. Simon ; M. Lemoal ; Y. AgidSource :
- Neuroscience [ 0306-4522 ] ; 1990.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Alzheimer Disease (metabolism), Alzheimer Disease (physiopathology), Animals, Brain Injuries (chemically induced), Brain Injuries (metabolism), Choline O-Acetyltransferase (metabolism), Female, Humans, Hydroxydopamines, Kinetics, Male, Neuromuscular Depolarizing Agents (metabolism), Oxadiazoles, Oxidopamine, Parkinson Disease (metabolism), Phencyclidine (analogs & derivatives), Phencyclidine (metabolism), Piperidines, Quisqualic Acid, Rats, Rats, Inbred Strains, Receptors, Neurotransmitter (metabolism), Receptors, Phencyclidine, Reference Values, Substantia Nigra (metabolism), Temporal Lobe (metabolism).
- MESH :
- chemical , analogs & derivatives : Phencyclidine.
- chemical , metabolism : Choline O-Acetyltransferase, Neuromuscular Depolarizing Agents, Phencyclidine, Receptors, Neurotransmitter.
- chemically induced : Brain Injuries.
- metabolism : Alzheimer Disease, Brain Injuries, Parkinson Disease, Substantia Nigra, Temporal Lobe.
- physiopathology : Alzheimer Disease.
- Aged, Aged, 80 and over, Animals, Female, Humans, Hydroxydopamines, Kinetics, Male, Oxadiazoles, Oxidopamine, Piperidines, Quisqualic Acid, Rats, Rats, Inbred Strains, Receptors, Phencyclidine, Reference Values.
Abstract
[3H]Vesamicol binding was characterized in human brain post mortem. The number of binding sites was then determined in parallel with choline acetyltransferase activity in the temporal cortex of patients with Alzheimer's disease, demented and non-demented patients with Parkinson's disease, and in the cerebral cortex of rats with quisqualic acid lesions of the nucleus basalis magnocellularis. Whereas choline acetyltransferase activity decreased in patients with Alzheimer's or Parkinson's disease indicating loss of cholinergic innervation, the number of binding sites for [3H]vesamicol was the same as or higher than in controls. Similar results were obtained with the lesioned rats. It is suggested that the increase in binding sites may reflect compensatory regulation of the spared neurons at the level of the synaptic vesicle.
PubMed: 2166243
Links to Exploration step
pubmed:2166243Le document en format XML
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Duyckaerts</name></author><author><name sortKey="Hauw, J J" sort="Hauw, J J" uniqKey="Hauw J" first="J J" last="Hauw">J J Hauw</name></author><author><name sortKey="Simon, H" sort="Simon, H" uniqKey="Simon H" first="H" last="Simon">H. Simon</name></author><author><name sortKey="Lemoal, M" sort="Lemoal, M" uniqKey="Lemoal M" first="M" last="Lemoal">M. Lemoal</name></author><author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y" last="Agid">Y. 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Agid</name></author></analytic><series><title level="j">Neuroscience</title><idno type="ISSN">0306-4522</idno><imprint><date when="1990" type="published">1990</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Alzheimer Disease (metabolism)</term><term>Alzheimer Disease (physiopathology)</term><term>Animals</term><term>Brain Injuries (chemically induced)</term><term>Brain Injuries (metabolism)</term><term>Choline O-Acetyltransferase (metabolism)</term><term>Female</term><term>Humans</term><term>Hydroxydopamines</term><term>Kinetics</term><term>Male</term><term>Neuromuscular Depolarizing Agents (metabolism)</term><term>Oxadiazoles</term><term>Oxidopamine</term><term>Parkinson Disease (metabolism)</term><term>Phencyclidine (analogs & derivatives)</term><term>Phencyclidine (metabolism)</term><term>Piperidines</term><term>Quisqualic Acid</term><term>Rats</term><term>Rats, Inbred Strains</term><term>Receptors, Neurotransmitter (metabolism)</term><term>Receptors, Phencyclidine</term><term>Reference Values</term><term>Substantia Nigra (metabolism)</term><term>Temporal Lobe (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Phencyclidine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Choline O-Acetyltransferase</term><term>Neuromuscular Depolarizing Agents</term><term>Phencyclidine</term><term>Receptors, Neurotransmitter</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Brain Injuries</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Alzheimer Disease</term><term>Brain Injuries</term><term>Parkinson Disease</term><term>Substantia Nigra</term><term>Temporal Lobe</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Alzheimer Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Animals</term><term>Female</term><term>Humans</term><term>Hydroxydopamines</term><term>Kinetics</term><term>Male</term><term>Oxadiazoles</term><term>Oxidopamine</term><term>Piperidines</term><term>Quisqualic Acid</term><term>Rats</term><term>Rats, Inbred Strains</term><term>Receptors, Phencyclidine</term><term>Reference Values</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">[3H]Vesamicol binding was characterized in human brain post mortem. The number of binding sites was then determined in parallel with choline acetyltransferase activity in the temporal cortex of patients with Alzheimer's disease, demented and non-demented patients with Parkinson's disease, and in the cerebral cortex of rats with quisqualic acid lesions of the nucleus basalis magnocellularis. Whereas choline acetyltransferase activity decreased in patients with Alzheimer's or Parkinson's disease indicating loss of cholinergic innervation, the number of binding sites for [3H]vesamicol was the same as or higher than in controls. Similar results were obtained with the lesioned rats. It is suggested that the increase in binding sites may reflect compensatory regulation of the spared neurons at the level of the synaptic vesicle.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">2166243</PMID><DateCreated><Year>1990</Year><Month>09</Month><Day>11</Day></DateCreated><DateCompleted><Year>1990</Year><Month>09</Month><Day>11</Day></DateCompleted><DateRevised><Year>2015</Year><Month>11</Month><Day>19</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0306-4522</ISSN><JournalIssue CitedMedium="Print"><Volume>35</Volume><Issue>2</Issue><PubDate><Year>1990</Year></PubDate></JournalIssue><Title>Neuroscience</Title><ISOAbbreviation>Neuroscience</ISOAbbreviation></Journal><ArticleTitle>Choline acetyltransferase activity and [3H]vesamicol binding in the temporal cortex of patients with Alzheimer's disease, Parkinson's disease, and rats with basal forebrain lesions.</ArticleTitle><Pagination><MedlinePgn>327-33</MedlinePgn></Pagination><Abstract><AbstractText>[3H]Vesamicol binding was characterized in human brain post mortem. The number of binding sites was then determined in parallel with choline acetyltransferase activity in the temporal cortex of patients with Alzheimer's disease, demented and non-demented patients with Parkinson's disease, and in the cerebral cortex of rats with quisqualic acid lesions of the nucleus basalis magnocellularis. Whereas choline acetyltransferase activity decreased in patients with Alzheimer's or Parkinson's disease indicating loss of cholinergic innervation, the number of binding sites for [3H]vesamicol was the same as or higher than in controls. Similar results were obtained with the lesioned rats. 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UI="D010622">Phencyclidine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000369" MajorTopicYN="N">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000544" MajorTopicYN="N">Alzheimer Disease</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001930" MajorTopicYN="N">Brain Injuries</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002795" MajorTopicYN="N">Choline 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