Time course of changes in striatal dopamine transporters and D2 receptors with specific iodinated markers in a rat model of Parkinson's disease.
Identifieur interne : 001242 ( PubMed/Checkpoint ); précédent : 001241; suivant : 001243Time course of changes in striatal dopamine transporters and D2 receptors with specific iodinated markers in a rat model of Parkinson's disease.
Auteurs : S. Chalon [France] ; P. Emond ; S. Bodard ; M P Vilar ; C. Thiercelin ; J C Besnard ; D. GuilloteauSource :
- Synapse (New York, N.Y.) [ 0887-4476 ] ; 1999.
English descriptors
- KwdEn :
- Animals, Benzamides, Carrier Proteins (metabolism), Corpus Striatum (diagnostic imaging), Dopamine (pharmacokinetics), Dopamine Antagonists (pharmacokinetics), Dopamine Plasma Membrane Transport Proteins, Iodine Radioisotopes (pharmacokinetics), Male, Membrane Glycoproteins, Membrane Transport Proteins, Nerve Tissue Proteins, Nortropanes (pharmacokinetics), Parkinson Disease (diagnostic imaging), Parkinson Disease (metabolism), Pyrrolidines, Radiopharmaceuticals (pharmacokinetics), Rats, Rats, Wistar, Receptors, Dopamine D2 (biosynthesis), Time Factors, Tomography, Emission-Computed, Single-Photon.
- MESH :
- chemical , biosynthesis : Receptors, Dopamine D2.
- chemical , metabolism : Carrier Proteins.
- chemical , pharmacokinetics : Dopamine, Dopamine Antagonists, Iodine Radioisotopes, Nortropanes, Radiopharmaceuticals.
- chemical : Benzamides, Dopamine Plasma Membrane Transport Proteins, Membrane Glycoproteins, Membrane Transport Proteins, Nerve Tissue Proteins, Pyrrolidines.
- diagnostic imaging : Corpus Striatum, Parkinson Disease.
- metabolism : Parkinson Disease.
- Animals, Male, Rats, Rats, Wistar, Time Factors, Tomography, Emission-Computed, Single-Photon.
Abstract
The time course of the loss in presynaptic dopamine transporters (DAT) and of the increase in postsynaptic dopamine D2 receptors (D2R) was studied in a rat model of Parkinson's disease. For this, in vitro autoradiographic experiments were performed in the striatum using (E)-N-(3-iodoprop-2-enyl)-2beta-carbomethoxy-3beta-(4'-methy lphenyl) nortropane (PE2I), a new single photon emission tomography (SPET) ligand for DAT, and iodobenzamide (IBZM), a SPET ligand for D2R. A significant decrease in [125I]PE2I binding was observed as early as 24 h after 6-hydroxydopamine lesion, whereas no change occurred in [125I]IBZM binding. At 48 h postlesion, PE2I binding was 50% decreased, while IBZM binding was 30% increased. Between 3 and 14 days postlesion, PE2I binding had almost totally disappeared and IBZM binding remained increased by around 40-50%. From these animal experiments, it can be assumed that PE2I would be very efficient for the detection of a reduction in the number of DAT reflecting neuronal loss, thus allowing early diagnosis of Parkinson's disease. The exploration of both DAT and D2R would improve follow-up of this disease.
DOI: 10.1002/(SICI)1098-2396(199902)31:2<134::AID-SYN6>3.0.CO;2-V
PubMed: 10024010
Affiliations:
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pubmed:10024010Le document en format XML
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Chalon</name><affiliation wicri:level="3"><nlm:affiliation>INSERM U316, Laboratoire de Biophysique Médicale et Pharmaceutique, Tours, France. chalon@balzac.univ-tours.fr</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>INSERM U316, Laboratoire de Biophysique Médicale et Pharmaceutique, Tours</wicri:regionArea><placeName><region type="region">Centre-Val de Loire</region><region type="old region">Région Centre</region><settlement type="city">Tours</settlement></placeName></affiliation></author><author><name sortKey="Emond, P" sort="Emond, P" uniqKey="Emond P" first="P" last="Emond">P. Emond</name></author><author><name sortKey="Bodard, S" sort="Bodard, S" uniqKey="Bodard S" first="S" last="Bodard">S. Bodard</name></author><author><name sortKey="Vilar, M P" sort="Vilar, M P" uniqKey="Vilar M" first="M P" last="Vilar">M P Vilar</name></author><author><name sortKey="Thiercelin, C" sort="Thiercelin, C" uniqKey="Thiercelin C" first="C" last="Thiercelin">C. Thiercelin</name></author><author><name sortKey="Besnard, J C" sort="Besnard, J C" uniqKey="Besnard J" first="J C" last="Besnard">J C Besnard</name></author><author><name sortKey="Guilloteau, D" sort="Guilloteau, D" uniqKey="Guilloteau D" first="D" last="Guilloteau">D. Guilloteau</name></author></analytic><series><title level="j">Synapse (New York, N.Y.)</title><idno type="ISSN">0887-4476</idno><imprint><date when="1999" type="published">1999</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Benzamides</term><term>Carrier Proteins (metabolism)</term><term>Corpus Striatum (diagnostic imaging)</term><term>Dopamine (pharmacokinetics)</term><term>Dopamine Antagonists (pharmacokinetics)</term><term>Dopamine Plasma Membrane Transport Proteins</term><term>Iodine Radioisotopes (pharmacokinetics)</term><term>Male</term><term>Membrane Glycoproteins</term><term>Membrane Transport Proteins</term><term>Nerve Tissue Proteins</term><term>Nortropanes (pharmacokinetics)</term><term>Parkinson Disease (diagnostic imaging)</term><term>Parkinson Disease (metabolism)</term><term>Pyrrolidines</term><term>Radiopharmaceuticals (pharmacokinetics)</term><term>Rats</term><term>Rats, Wistar</term><term>Receptors, Dopamine D2 (biosynthesis)</term><term>Time Factors</term><term>Tomography, Emission-Computed, Single-Photon</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Receptors, Dopamine D2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Carrier Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacokinetics" xml:lang="en"><term>Dopamine</term><term>Dopamine Antagonists</term><term>Iodine Radioisotopes</term><term>Nortropanes</term><term>Radiopharmaceuticals</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Benzamides</term><term>Dopamine Plasma Membrane Transport Proteins</term><term>Membrane Glycoproteins</term><term>Membrane Transport Proteins</term><term>Nerve Tissue Proteins</term><term>Pyrrolidines</term></keywords><keywords scheme="MESH" qualifier="diagnostic imaging" xml:lang="en"><term>Corpus Striatum</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Male</term><term>Rats</term><term>Rats, Wistar</term><term>Time Factors</term><term>Tomography, Emission-Computed, Single-Photon</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The time course of the loss in presynaptic dopamine transporters (DAT) and of the increase in postsynaptic dopamine D2 receptors (D2R) was studied in a rat model of Parkinson's disease. For this, in vitro autoradiographic experiments were performed in the striatum using (E)-N-(3-iodoprop-2-enyl)-2beta-carbomethoxy-3beta-(4'-methy lphenyl) nortropane (PE2I), a new single photon emission tomography (SPET) ligand for DAT, and iodobenzamide (IBZM), a SPET ligand for D2R. A significant decrease in [125I]PE2I binding was observed as early as 24 h after 6-hydroxydopamine lesion, whereas no change occurred in [125I]IBZM binding. At 48 h postlesion, PE2I binding was 50% decreased, while IBZM binding was 30% increased. Between 3 and 14 days postlesion, PE2I binding had almost totally disappeared and IBZM binding remained increased by around 40-50%. From these animal experiments, it can be assumed that PE2I would be very efficient for the detection of a reduction in the number of DAT reflecting neuronal loss, thus allowing early diagnosis of Parkinson's disease. The exploration of both DAT and D2R would improve follow-up of this disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">10024010</PMID><DateCreated><Year>1999</Year><Month>07</Month><Day>12</Day></DateCreated><DateCompleted><Year>1999</Year><Month>07</Month><Day>12</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>24</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0887-4476</ISSN><JournalIssue CitedMedium="Print"><Volume>31</Volume><Issue>2</Issue><PubDate><Year>1999</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Synapse (New York, N.Y.)</Title><ISOAbbreviation>Synapse</ISOAbbreviation></Journal><ArticleTitle>Time course of changes in striatal dopamine transporters and D2 receptors with specific iodinated markers in a rat model of Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>134-9</MedlinePgn></Pagination><Abstract><AbstractText>The time course of the loss in presynaptic dopamine transporters (DAT) and of the increase in postsynaptic dopamine D2 receptors (D2R) was studied in a rat model of Parkinson's disease. For this, in vitro autoradiographic experiments were performed in the striatum using (E)-N-(3-iodoprop-2-enyl)-2beta-carbomethoxy-3beta-(4'-methy lphenyl) nortropane (PE2I), a new single photon emission tomography (SPET) ligand for DAT, and iodobenzamide (IBZM), a SPET ligand for D2R. A significant decrease in [125I]PE2I binding was observed as early as 24 h after 6-hydroxydopamine lesion, whereas no change occurred in [125I]IBZM binding. At 48 h postlesion, PE2I binding was 50% decreased, while IBZM binding was 30% increased. Between 3 and 14 days postlesion, PE2I binding had almost totally disappeared and IBZM binding remained increased by around 40-50%. From these animal experiments, it can be assumed that PE2I would be very efficient for the detection of a reduction in the number of DAT reflecting neuronal loss, thus allowing early diagnosis of Parkinson's disease. 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Single-Photon</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1999</Year><Month>2</Month><Day>19</Day><Hour>4</Hour><Minute>31</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2000</Year><Month>6</Month><Day>20</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1999</Year><Month>2</Month><Day>19</Day><Hour>4</Hour><Minute>31</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">10024010</ArticleId><ArticleId IdType="pii">10.1002/(SICI)1098-2396(199902)31:2<134::AID-SYN6>3.0.CO;2-V</ArticleId><ArticleId IdType="doi">10.1002/(SICI)1098-2396(199902)31:2<134::AID-SYN6>3.0.CO;2-V</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>France</li></country><region><li>Centre-Val de Loire</li><li>Région Centre</li></region><settlement><li>Tours</li></settlement></list><tree><noCountry><name sortKey="Besnard, J C" sort="Besnard, J C" uniqKey="Besnard J" first="J C" last="Besnard">J C Besnard</name><name sortKey="Bodard, S" sort="Bodard, S" uniqKey="Bodard S" first="S" last="Bodard">S. Bodard</name><name sortKey="Emond, P" sort="Emond, P" uniqKey="Emond P" first="P" last="Emond">P. Emond</name><name sortKey="Guilloteau, D" sort="Guilloteau, D" uniqKey="Guilloteau D" first="D" last="Guilloteau">D. Guilloteau</name><name sortKey="Thiercelin, C" sort="Thiercelin, C" uniqKey="Thiercelin C" first="C" last="Thiercelin">C. Thiercelin</name><name sortKey="Vilar, M P" sort="Vilar, M P" uniqKey="Vilar M" first="M P" last="Vilar">M P Vilar</name></noCountry><country name="France"><region name="Centre-Val de Loire"><name sortKey="Chalon, S" sort="Chalon, S" uniqKey="Chalon S" first="S" last="Chalon">S. Chalon</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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