Electroconvulsive shock enhances striatal dopamine D1 and D3 receptor binding and improves motor performance in 6-OHDA-lesioned rats
Identifieur interne : 000142 ( Ncbi/Merge ); précédent : 000141; suivant : 000143Electroconvulsive shock enhances striatal dopamine D1 and D3 receptor binding and improves motor performance in 6-OHDA-lesioned rats
Auteurs : Elissa Strome ; Athanasios Zis ; Doris DoudetSource :
- Journal of Psychiatry & Neuroscience [ 1180-4882 ] ; 2007.
Abstract
Electroconvulsive therapy (ECT) is a widely used and effective treatment for mood disorders and appears to have positive effects on the motor symptoms of Parkinson's disease (PD), improving motor function for several weeks. Because repeated electroconvulsive shock (ECS) in normal animals enhances striatal dopamine (DA) D1 and D3 receptor binding, we hypothesized that upregulation of D1 and D3 receptors may also be occurring in the parkinsonian brain after repeated ECS treatment.
Rats were rendered hemiparkinsonian through unilateral infusion of the DA-specific neurotoxin 6-hydroxydopamine into the medial forebrain bundle and substantia nigra. The animals were tested for hindlimb and forelimb function before and 48 hours after the last of 10 daily treatments with ECS or sham. After sacrifice, DA receptor binding was determined autoradiographically.
While there was no increase in forelimb use in the cylinder test, ECS treatment significantly improved hindlimb motor performance on a tapered beam-walking test and enhanced striatal D1 and D3 receptor binding, without affecting D2 receptor binding.
This study suggests that at least part of the mechanism of action of ECT in PD may be enhanced DA function within the direct pathway of the basal ganglia and may support the further study and use of ECT as a potential adjunct treatment for PD.
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PubMed: 17476366
PubMed Central: 1863551
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Electroconvulsive shock enhances striatal dopamine D<sub>1</sub> and D<sub>3</sub> receptor binding and improves motor performance in 6-OHDA-lesioned rats</title><author><name sortKey="Strome, Elissa M" sort="Strome, Elissa M" uniqKey="Strome E" first="Elissa" last="Strome">Elissa Strome</name></author><author><name sortKey="Zis, Athanasios P" sort="Zis, Athanasios P" uniqKey="Zis A" first="Athanasios" last="Zis">Athanasios Zis</name></author><author><name sortKey="Doudet, Doris J" sort="Doudet, Doris J" uniqKey="Doudet D" first="Doris" last="Doudet">Doris Doudet</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">17476366</idno><idno type="pmc">1863551</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1863551</idno><idno type="RBID">PMC:1863551</idno><date when="2007">2007</date><idno type="wicri:Area/Pmc/Corpus">000092</idno><idno type="wicri:Area/Pmc/Curation">000092</idno><idno type="wicri:Area/Pmc/Checkpoint">000249</idno><idno type="wicri:Area/Ncbi/Merge">000142</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Electroconvulsive shock enhances striatal dopamine D<sub>1</sub> and D<sub>3</sub> receptor binding and improves motor performance in 6-OHDA-lesioned rats</title><author><name sortKey="Strome, Elissa M" sort="Strome, Elissa M" uniqKey="Strome E" first="Elissa" last="Strome">Elissa Strome</name></author><author><name sortKey="Zis, Athanasios P" sort="Zis, Athanasios P" uniqKey="Zis A" first="Athanasios" last="Zis">Athanasios Zis</name></author><author><name sortKey="Doudet, Doris J" sort="Doudet, Doris J" uniqKey="Doudet D" first="Doris" last="Doudet">Doris Doudet</name></author></analytic><series><title level="j">Journal of Psychiatry & Neuroscience</title><idno type="ISSN">1180-4882</idno><idno type="e-ISSN">1488-2434</idno><imprint><date when="2007">2007</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec><title>Objective</title><p>Electroconvulsive therapy (ECT) is a widely used and effective treatment for mood disorders and appears to have positive effects on the motor symptoms of Parkinson's disease (PD), improving motor function for several weeks. Because repeated electroconvulsive shock (ECS) in normal animals enhances striatal dopamine (DA) D<sub>1</sub> and D<sub>3</sub> receptor binding, we hypothesized that upregulation of D<sub>1</sub> and D<sub>3</sub> receptors may also be occurring in the parkinsonian brain after repeated ECS treatment.</p></sec><sec><title>Methods</title><p>Rats were rendered hemiparkinsonian through unilateral infusion of the DA-specific neurotoxin 6-hydroxydopamine into the medial forebrain bundle and substantia nigra. The animals were tested for hindlimb and forelimb function before and 48 hours after the last of 10 daily treatments with ECS or sham. After sacrifice, DA receptor binding was determined autoradiographically.</p></sec><sec><title>Results</title><p>While there was no increase in forelimb use in the cylinder test, ECS treatment significantly improved hindlimb motor performance on a tapered beam-walking test and enhanced striatal D<sub>1</sub> and D<sub>3</sub> receptor binding, without affecting D<sub>2</sub> receptor binding.</p></sec><sec><title>Conclusion</title><p>This study suggests that at least part of the mechanism of action of ECT in PD may be enhanced DA function within the direct pathway of the basal ganglia and may support the further study and use of ECT as a potential adjunct treatment for PD.</p></sec></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">J Psychiatry Neurosci</journal-id><journal-id journal-id-type="publisher-id">Journal of Psychiatry & Neuroscience</journal-id><journal-title>Journal of Psychiatry & Neuroscience</journal-title><issn pub-type="ppub">1180-4882</issn><issn pub-type="epub">1488-2434</issn></journal-meta><article-meta><article-id pub-id-type="pmid">17476366</article-id><article-id pub-id-type="pmc">1863551</article-id><article-id pub-id-type="publisher-id">0001585-200705000-00005</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Paper</subject></subj-group></article-categories><title-group><article-title>Electroconvulsive shock enhances striatal dopamine D<sub>1</sub> and D<sub>3</sub> receptor binding and improves motor performance in 6-OHDA-lesioned rats</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Strome</surname><given-names>Elissa M.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Zis</surname><given-names>Athanasios P.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Doudet</surname><given-names>Doris J.</given-names></name></contrib></contrib-group><aff>Strome and Doudet — Pacific Parkinson's Research Centre; Zis — Department of Psychiatry, University of British Columbia, Vancouver, BC<break></break></aff><pub-date pub-type="ppub"><month>5</month><year>2007</year></pub-date><volume>32</volume><issue>3</issue><fpage>193</fpage><lpage>202</lpage><copyright-statement>© 2007 Canadian Medical Association</copyright-statement><abstract><sec><title>Objective</title><p>Electroconvulsive therapy (ECT) is a widely used and effective treatment for mood disorders and appears to have positive effects on the motor symptoms of Parkinson's disease (PD), improving motor function for several weeks. Because repeated electroconvulsive shock (ECS) in normal animals enhances striatal dopamine (DA) D<sub>1</sub> and D<sub>3</sub> receptor binding, we hypothesized that upregulation of D<sub>1</sub> and D<sub>3</sub> receptors may also be occurring in the parkinsonian brain after repeated ECS treatment.</p></sec><sec><title>Methods</title><p>Rats were rendered hemiparkinsonian through unilateral infusion of the DA-specific neurotoxin 6-hydroxydopamine into the medial forebrain bundle and substantia nigra. The animals were tested for hindlimb and forelimb function before and 48 hours after the last of 10 daily treatments with ECS or sham. After sacrifice, DA receptor binding was determined autoradiographically.</p></sec><sec><title>Results</title><p>While there was no increase in forelimb use in the cylinder test, ECS treatment significantly improved hindlimb motor performance on a tapered beam-walking test and enhanced striatal D<sub>1</sub> and D<sub>3</sub> receptor binding, without affecting D<sub>2</sub> receptor binding.</p></sec><sec><title>Conclusion</title><p>This study suggests that at least part of the mechanism of action of ECT in PD may be enhanced DA function within the direct pathway of the basal ganglia and may support the further study and use of ECT as a potential adjunct treatment for PD.</p></sec></abstract><trans-abstract xml:lang="fre"><sec><title>Objectif</title><p>L'électrochoc est un traitement très répandu et efficace contre les troubles de l'humeur et il semble avoir des effets positifs sur les symptômes de la maladie de Parkinson (MP) qui touchent la motricité, car il améliore la fonction motrice pendant plusieurs semaines. Parce que l'électrochoc à répétition chez des animaux normaux améliore la fixation aux récepteurs D<sub>1</sub> et D<sub>3</sub> de la dopamine striatale, nous avons posé en hypothèse qu'il peut y avoir aussi régulation à la hausse des récepteurs D<sub>1</sub> et D<sub>3</sub> dans un cerveau parkinsonien après des électrochocs à répétition.</p></sec><sec><title>Méthodes</title><p>On a rendu des rats hémiparkinsoniens par perfusion unilatérale de neurotoxine 6-hydroxydopamine spécifique à la dopamine dans le faisceau médian du cerveau antérieur et les substances noires. On a vérifié le fonctionnement des pattes arrière et avant des animaux avant et 48 heures après 10 traitements quotidiens d'électrochoc ou traitements factices. Après le sacrifice, on a déterminé par autoradiographie qu'il y avait fixation aux récepteurs de la dopamine.</p></sec><sec><title>Résultats</title><p>Même si les sujets n'ont pas utilisé davantage leurs pattes avant au cours du test du cylindre, l'électrochoc a amélioré considérablement la performance motrice des pattes arrière au cours du test de la poutre en queue de billard et a amélioré la fixation aux récepteurs D<sub>1</sub> et D<sub>3</sub> de la dopamine striatale sans avoir d'effet sur la fixation aux récepteurs D<sub>2</sub>.</p></sec><sec><title>Conclusion</title><p>Cette étude indique que le mécanisme d'action de l'électrochoc dans les cas de MP peut consister en partie à améliorer la fonction de la dopamine par la voie directe des noyaux gris centraux et pourrait appuyer une étude plus poussée et l'utilisation de l'électrochoc comme traitement d'appoint éventuel contre la MP.</p></sec></trans-abstract><kwd-group><title>Medical subject headings</title><kwd>dopamine receptors</kwd><kwd>electroconvulsive therapy</kwd><kwd>motor skills</kwd><kwd>Parkinson disease</kwd></kwd-group></article-meta></front></pmc><affiliations><list></list><tree><noCountry><name sortKey="Doudet, Doris J" sort="Doudet, Doris J" uniqKey="Doudet D" first="Doris" last="Doudet">Doris Doudet</name><name sortKey="Strome, Elissa M" sort="Strome, Elissa M" uniqKey="Strome E" first="Elissa" last="Strome">Elissa Strome</name><name sortKey="Zis, Athanasios P" sort="Zis, Athanasios P" uniqKey="Zis A" first="Athanasios" last="Zis">Athanasios Zis</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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