I2-imidazoline binding sites and monoamine oxidase activity in human postmortem brain from patients with Parkinson's disease.
Identifieur interne : 001399 ( PubMed/Checkpoint ); précédent : 001398; suivant : 001400I2-imidazoline binding sites and monoamine oxidase activity in human postmortem brain from patients with Parkinson's disease.
Auteurs : C. Gargalidis-Moudanos [France] ; N. Pizzinat ; F. Javoy-Agid ; A. Remaury ; A. PariniSource :
- Neurochemistry international [ 0197-0186 ] ; 1997.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Brain (metabolism), Cerebral Cortex (metabolism), Cerebral Cortex (ultrastructure), Female, Humans, Idazoxan (metabolism), Imidazoline Receptors, Male, Mitochondria (metabolism), Monoamine Oxidase (metabolism), Parkinson Disease (metabolism), Phenethylamines (metabolism), Postmortem Changes, Putamen (metabolism), Putamen (ultrastructure), Receptors, Drug (metabolism), Tritium, Tyramine (metabolism).
- MESH :
- chemical , metabolism : Idazoxan, Monoamine Oxidase, Phenethylamines, Receptors, Drug, Tyramine.
- metabolism : Brain, Cerebral Cortex, Mitochondria, Parkinson Disease, Putamen.
- ultrastructure : Cerebral Cortex, Putamen.
- Aged, Aged, 80 and over, Female, Humans, Imidazoline Receptors, Male, Postmortem Changes, Tritium.
Abstract
I2-imidazoline binding site (I2BS) has been identified with a regulatory site located on a sub-population of monoamine oxidase (MAO)-A and -B. Previous studies showed a modification of MAO and I2BS in the elderly and in neurodegenerative processes such as Alzheimer's disease. In the present study, we studied the potential modification of I2 binding sites and monoamine oxidases in Parkinson's disease. Putamen and cerebral cortex were collected from 17 normal subjects (79 +/- 12 yr) and 16 patients (76 +/- 9 yr) affected by Parkinson's disease. In mitochondrial preparations, radioligand binding studies with [3H]idazoxan showed that putamen and frontal cortex express equivalent amount of I2BS. The density and affinity of I2BS were similar in normal subjects (putamen: Bmax = 207 +/- 58 fmol/mg of protein, Kd = 10.1 +/- 3.4 nM; cerebral cortex: Bmax = 193 +/- 54 fmol/mg of protein, Kd = 12.8 +/- 6.8 nM) and Parkinson's disease patients (putamen: Bmax = 193 +/- 60 fmol/mg of protein, Kd = 9.8 +/- 4.6 nM; cerebral cortex: Bmax = 199 +/- 49 fmol/mg of protein, Kd = 15.9 +/- 8.1 nM). The activity of total monoamine oxidase and monoamine oxidase B, measured by [14C]tyramine and [14C]phenylethylamine oxidation, respectively, were higher in putamen than in cerebral cortex. No differences have been detected in the enzyme activity between normal and pathological subjects. These data suggest that, although MAO and I2BS may play a role in the development of Parkinson's disease, they are not altered in the chronic phase of this disease.
PubMed: 9116585
Affiliations:
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Gargalidis-Moudanos</name><affiliation wicri:level="3"><nlm:affiliation>INSERM U388, Institut Louis Bugnard, CHU Rangueil, Toulouse, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>INSERM U388, Institut Louis Bugnard, CHU Rangueil, Toulouse</wicri:regionArea><placeName><region type="region">Occitanie (région administrative)</region><region type="old region">Midi-Pyrénées</region><settlement type="city">Toulouse</settlement></placeName></affiliation></author><author><name sortKey="Pizzinat, N" sort="Pizzinat, N" uniqKey="Pizzinat N" first="N" last="Pizzinat">N. Pizzinat</name></author><author><name sortKey="Javoy Agid, F" sort="Javoy Agid, F" uniqKey="Javoy Agid F" first="F" last="Javoy-Agid">F. Javoy-Agid</name></author><author><name sortKey="Remaury, A" sort="Remaury, A" uniqKey="Remaury A" first="A" last="Remaury">A. Remaury</name></author><author><name sortKey="Parini, A" sort="Parini, A" uniqKey="Parini A" first="A" last="Parini">A. Parini</name></author></analytic><series><title level="j">Neurochemistry international</title><idno type="ISSN">0197-0186</idno><imprint><date when="1997" type="published">1997</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Brain (metabolism)</term><term>Cerebral Cortex (metabolism)</term><term>Cerebral Cortex (ultrastructure)</term><term>Female</term><term>Humans</term><term>Idazoxan (metabolism)</term><term>Imidazoline Receptors</term><term>Male</term><term>Mitochondria (metabolism)</term><term>Monoamine Oxidase (metabolism)</term><term>Parkinson Disease (metabolism)</term><term>Phenethylamines (metabolism)</term><term>Postmortem Changes</term><term>Putamen (metabolism)</term><term>Putamen (ultrastructure)</term><term>Receptors, Drug (metabolism)</term><term>Tritium</term><term>Tyramine (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Idazoxan</term><term>Monoamine Oxidase</term><term>Phenethylamines</term><term>Receptors, Drug</term><term>Tyramine</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Brain</term><term>Cerebral Cortex</term><term>Mitochondria</term><term>Parkinson Disease</term><term>Putamen</term></keywords><keywords scheme="MESH" qualifier="ultrastructure" xml:lang="en"><term>Cerebral Cortex</term><term>Putamen</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Female</term><term>Humans</term><term>Imidazoline Receptors</term><term>Male</term><term>Postmortem Changes</term><term>Tritium</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">I2-imidazoline binding site (I2BS) has been identified with a regulatory site located on a sub-population of monoamine oxidase (MAO)-A and -B. Previous studies showed a modification of MAO and I2BS in the elderly and in neurodegenerative processes such as Alzheimer's disease. In the present study, we studied the potential modification of I2 binding sites and monoamine oxidases in Parkinson's disease. Putamen and cerebral cortex were collected from 17 normal subjects (79 +/- 12 yr) and 16 patients (76 +/- 9 yr) affected by Parkinson's disease. In mitochondrial preparations, radioligand binding studies with [3H]idazoxan showed that putamen and frontal cortex express equivalent amount of I2BS. The density and affinity of I2BS were similar in normal subjects (putamen: Bmax = 207 +/- 58 fmol/mg of protein, Kd = 10.1 +/- 3.4 nM; cerebral cortex: Bmax = 193 +/- 54 fmol/mg of protein, Kd = 12.8 +/- 6.8 nM) and Parkinson's disease patients (putamen: Bmax = 193 +/- 60 fmol/mg of protein, Kd = 9.8 +/- 4.6 nM; cerebral cortex: Bmax = 199 +/- 49 fmol/mg of protein, Kd = 15.9 +/- 8.1 nM). The activity of total monoamine oxidase and monoamine oxidase B, measured by [14C]tyramine and [14C]phenylethylamine oxidation, respectively, were higher in putamen than in cerebral cortex. No differences have been detected in the enzyme activity between normal and pathological subjects. These data suggest that, although MAO and I2BS may play a role in the development of Parkinson's disease, they are not altered in the chronic phase of this disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">9116585</PMID><DateCreated><Year>1997</Year><Month>04</Month><Day>24</Day></DateCreated><DateCompleted><Year>1997</Year><Month>04</Month><Day>24</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0197-0186</ISSN><JournalIssue CitedMedium="Print"><Volume>30</Volume><Issue>1</Issue><PubDate><Year>1997</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Neurochemistry international</Title><ISOAbbreviation>Neurochem. Int.</ISOAbbreviation></Journal><ArticleTitle>I2-imidazoline binding sites and monoamine oxidase activity in human postmortem brain from patients with Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>31-6</MedlinePgn></Pagination><Abstract><AbstractText>I2-imidazoline binding site (I2BS) has been identified with a regulatory site located on a sub-population of monoamine oxidase (MAO)-A and -B. Previous studies showed a modification of MAO and I2BS in the elderly and in neurodegenerative processes such as Alzheimer's disease. In the present study, we studied the potential modification of I2 binding sites and monoamine oxidases in Parkinson's disease. Putamen and cerebral cortex were collected from 17 normal subjects (79 +/- 12 yr) and 16 patients (76 +/- 9 yr) affected by Parkinson's disease. In mitochondrial preparations, radioligand binding studies with [3H]idazoxan showed that putamen and frontal cortex express equivalent amount of I2BS. The density and affinity of I2BS were similar in normal subjects (putamen: Bmax = 207 +/- 58 fmol/mg of protein, Kd = 10.1 +/- 3.4 nM; cerebral cortex: Bmax = 193 +/- 54 fmol/mg of protein, Kd = 12.8 +/- 6.8 nM) and Parkinson's disease patients (putamen: Bmax = 193 +/- 60 fmol/mg of protein, Kd = 9.8 +/- 4.6 nM; cerebral cortex: Bmax = 199 +/- 49 fmol/mg of protein, Kd = 15.9 +/- 8.1 nM). The activity of total monoamine oxidase and monoamine oxidase B, measured by [14C]tyramine and [14C]phenylethylamine oxidation, respectively, were higher in putamen than in cerebral cortex. No differences have been detected in the enzyme activity between normal and pathological subjects. These data suggest that, although MAO and I2BS may play a role in the development of Parkinson's disease, they are not altered in the chronic phase of this disease.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gargalidis-Moudanos</LastName><ForeName>C</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>INSERM U388, Institut Louis Bugnard, CHU Rangueil, Toulouse, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pizzinat</LastName><ForeName>N</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Javoy-Agid</LastName><ForeName>F</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Remaury</LastName><ForeName>A</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Parini</LastName><ForeName>A</ForeName><Initials>A</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>England</Country><MedlineTA>Neurochem Int</MedlineTA><NlmUniqueID>8006959</NlmUniqueID><ISSNLinking>0197-0186</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054755">Imidazoline Receptors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010627">Phenethylamines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011955">Receptors, Drug</NameOfSubstance></Chemical><Chemical><RegistryNumber>10028-17-8</RegistryNumber><NameOfSubstance UI="D014316">Tritium</NameOfSubstance></Chemical><Chemical><RegistryNumber>327C7L2BXQ</RegistryNumber><NameOfSubstance UI="C029261">phenethylamine</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.4.3.4</RegistryNumber><NameOfSubstance UI="D008995">Monoamine Oxidase</NameOfSubstance></Chemical><Chemical><RegistryNumber>X8ZC7V0OX3</RegistryNumber><NameOfSubstance UI="D014439">Tyramine</NameOfSubstance></Chemical><Chemical><RegistryNumber>Y310PA316B</RegistryNumber><NameOfSubstance UI="D019329">Idazoxan</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="D001921" MajorTopicYN="N">Brain</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002540" MajorTopicYN="N">Cerebral Cortex</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000648" MajorTopicYN="N">ultrastructure</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019329" MajorTopicYN="N">Idazoxan</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054755" MajorTopicYN="N">Imidazoline Receptors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008928" MajorTopicYN="N">Mitochondria</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008995" MajorTopicYN="N">Monoamine Oxidase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010627" MajorTopicYN="N">Phenethylamines</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011180" MajorTopicYN="N">Postmortem Changes</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011699" MajorTopicYN="N">Putamen</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000648" MajorTopicYN="N">ultrastructure</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011955" MajorTopicYN="N">Receptors, Drug</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014316" MajorTopicYN="N">Tritium</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014439" MajorTopicYN="N">Tyramine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1997</Year><Month>1</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1997</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1997</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">9116585</ArticleId><ArticleId IdType="pii">S0197018696000356</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>France</li></country><region><li>Midi-Pyrénées</li><li>Occitanie (région administrative)</li></region><settlement><li>Toulouse</li></settlement></list><tree><noCountry><name sortKey="Javoy Agid, F" sort="Javoy Agid, F" uniqKey="Javoy Agid F" first="F" last="Javoy-Agid">F. Javoy-Agid</name><name sortKey="Parini, A" sort="Parini, A" uniqKey="Parini A" first="A" last="Parini">A. Parini</name><name sortKey="Pizzinat, N" sort="Pizzinat, N" uniqKey="Pizzinat N" first="N" last="Pizzinat">N. Pizzinat</name><name sortKey="Remaury, A" sort="Remaury, A" uniqKey="Remaury A" first="A" last="Remaury">A. Remaury</name></noCountry><country name="France"><region name="Occitanie (région administrative)"><name sortKey="Gargalidis Moudanos, C" sort="Gargalidis Moudanos, C" uniqKey="Gargalidis Moudanos C" first="C" last="Gargalidis-Moudanos">C. Gargalidis-Moudanos</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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