Levodopa enhances synaptic plasticity in the substantia nigra pars reticulata of Parkinson's disease patients
Identifieur interne : 000573 ( PascalFrancis/Corpus ); précédent : 000572; suivant : 000574Levodopa enhances synaptic plasticity in the substantia nigra pars reticulata of Parkinson's disease patients
Auteurs : I. A. Prescott ; J. O. Dostrovsky ; E. Moro ; M. Hodaie ; A. M. Lozano ; W. D. HutchisonSource :
- Brain [ 0006-8950 ] ; 2009.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
Parkinson's disease, caused by the loss of dopaminergic nigrostriatal projections, is a debilitating neurodegenerative disease characterized by bradykinesia, rigidity, tremor and postural instability. The dopamine precursor levodopa (L-dopa) is the most effective treatment for the amelioration of Parkinson's disease signs and symptoms, but long-term administration can lead to disabling motor fluctuations and L-dopa -induced dyskinesias (LIDs). Studies in rat striatal slices have shown dopamine to be an essential component of activity-dependent synaptic plasticity at the input to the basal ganglia, but dopamine is also released from ventrally projecting dendrites of the substantia nigra pars compacta (SNc) on the substantia nigra pars reticulata (SNr), a major output structure of the basal ganglia. We characterized synaptic plasticity in the SNr using field potentials evoked with a nearby microelectrode (fEPs), in 18 Parkinson's disease patients undergoing implantation of deep brain stimulating (DBS) electrodes in the subthalamic nucleus (STN). High frequency stimulation (HFS-four trains of 2s at 100 Hz) in the SNr failed to induce a lasting change in test fEPs (1 Hz) amplitudes in patients OFF medication (decayed to baseline by 160s). Following oral L-dopa administration, HFS induced a potentiation of the fEP amplitudes (+29.3% of baseline at 160s following a plateau). Our findings suggest that extrastriatal dopamine modulates activity-dependent synaptic plasticity at basal ganglia output neurons. Dopamine medication state clearly impacts fEP amplitude, and the lasting nature of the increase is reminiscent of LTP-like changes, indicating that aberrant synaptic plasticity may play a role in the pathophysiology of Parkinson's disease.
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Format Inist (serveur)
| NO : | PASCAL 09-0108581 INIST |
|---|---|
| ET : | Levodopa enhances synaptic plasticity in the substantia nigra pars reticulata of Parkinson's disease patients |
| AU : | PRESCOTT (I. A.); DOSTROVSKY (J. O.); MORO (E.); HODAIE (M.); LOZANO (A. M.); HUTCHISON (W. D.) |
| AF : | Department of Physiology, University of Toronto/Canada (1 aut., 2 aut., 6 aut.); Division of Neurosurgery, Department of Surgery, Toronto Western Research Institute and Krembil Neuroscience Centre/Canada (2 aut., 3 aut., 4 aut., 5 aut., 6 aut.) |
| DT : | Publication en série; Niveau analytique |
| SO : | Brain; ISSN 0006-8950; Royaume-Uni; Da. 2009; Vol. 132; No. p. 2; Pp. 309-318; Bibl. 1 p.1/4 |
| LA : | Anglais |
| EA : | Parkinson's disease, caused by the loss of dopaminergic nigrostriatal projections, is a debilitating neurodegenerative disease characterized by bradykinesia, rigidity, tremor and postural instability. The dopamine precursor levodopa (L-dopa) is the most effective treatment for the amelioration of Parkinson's disease signs and symptoms, but long-term administration can lead to disabling motor fluctuations and L-dopa -induced dyskinesias (LIDs). Studies in rat striatal slices have shown dopamine to be an essential component of activity-dependent synaptic plasticity at the input to the basal ganglia, but dopamine is also released from ventrally projecting dendrites of the substantia nigra pars compacta (SNc) on the substantia nigra pars reticulata (SNr), a major output structure of the basal ganglia. We characterized synaptic plasticity in the SNr using field potentials evoked with a nearby microelectrode (fEPs), in 18 Parkinson's disease patients undergoing implantation of deep brain stimulating (DBS) electrodes in the subthalamic nucleus (STN). High frequency stimulation (HFS-four trains of 2s at 100 Hz) in the SNr failed to induce a lasting change in test fEPs (1 Hz) amplitudes in patients OFF medication (decayed to baseline by 160s). Following oral L-dopa administration, HFS induced a potentiation of the fEP amplitudes (+29.3% of baseline at 160s following a plateau). Our findings suggest that extrastriatal dopamine modulates activity-dependent synaptic plasticity at basal ganglia output neurons. Dopamine medication state clearly impacts fEP amplitude, and the lasting nature of the increase is reminiscent of LTP-like changes, indicating that aberrant synaptic plasticity may play a role in the pathophysiology of Parkinson's disease. |
| CC : | 002B17; 002B17G |
| FD : | Maladie de Parkinson; Pathologie du système nerveux; Lévodopa; Plasticité synaptique; Locus niger; Homme; Microélectrode; Noyau gris central |
| FG : | Encéphale; Système nerveux central; Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du système nerveux central |
| ED : | Parkinson disease; Nervous system diseases; Levodopa; Synaptic plasticity; Locus niger; Human; Microelectrode; Basal ganglion |
| EG : | Encephalon; Central nervous system; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease |
| SD : | Parkinson enfermedad; Sistema nervioso patología; Levodopa; Plasticidad sináptica; Locus níger; Hombre; Microeléctrodo; Núcleo basal |
| LO : | INIST-998.354000185402950040 |
| ID : | 09-0108581 |
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A." last="Prescott">I. A. Prescott</name><affiliation><inist:fA14 i1="01"><s1>Department of Physiology, University of Toronto</s1><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>6 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Dostrovsky, J O" sort="Dostrovsky, J O" uniqKey="Dostrovsky J" first="J. O." last="Dostrovsky">J. O. Dostrovsky</name><affiliation><inist:fA14 i1="01"><s1>Department of Physiology, University of Toronto</s1><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>6 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>Division of Neurosurgery, Department of Surgery, Toronto Western Research Institute and Krembil Neuroscience Centre</s1><s3>CAN</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Moro, E" sort="Moro, E" uniqKey="Moro E" first="E." last="Moro">E. Moro</name><affiliation><inist:fA14 i1="02"><s1>Division of Neurosurgery, Department of Surgery, Toronto Western Research Institute and Krembil Neuroscience Centre</s1><s3>CAN</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Hodaie, M" sort="Hodaie, M" uniqKey="Hodaie M" first="M." last="Hodaie">M. Hodaie</name><affiliation><inist:fA14 i1="02"><s1>Division of Neurosurgery, Department of Surgery, Toronto Western Research Institute and Krembil Neuroscience Centre</s1><s3>CAN</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Lozano, A M" sort="Lozano, A M" uniqKey="Lozano A" first="A. M." last="Lozano">A. M. Lozano</name><affiliation><inist:fA14 i1="02"><s1>Division of Neurosurgery, Department of Surgery, Toronto Western Research Institute and Krembil Neuroscience Centre</s1><s3>CAN</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Hutchison, W D" sort="Hutchison, W D" uniqKey="Hutchison W" first="W. D." last="Hutchison">W. D. Hutchison</name><affiliation><inist:fA14 i1="01"><s1>Department of Physiology, University of Toronto</s1><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>6 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>Division of Neurosurgery, Department of Surgery, Toronto Western Research Institute and Krembil Neuroscience Centre</s1><s3>CAN</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14></affiliation></author></analytic><series><title level="j" type="main">Brain</title><title level="j" type="abbreviated">Brain</title><idno type="ISSN">0006-8950</idno><imprint><date when="2009">2009</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Brain</title><title level="j" type="abbreviated">Brain</title><idno type="ISSN">0006-8950</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Basal ganglion</term><term>Human</term><term>Levodopa</term><term>Locus niger</term><term>Microelectrode</term><term>Nervous system diseases</term><term>Parkinson disease</term><term>Synaptic plasticity</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Maladie de Parkinson</term><term>Pathologie du système nerveux</term><term>Lévodopa</term><term>Plasticité synaptique</term><term>Locus niger</term><term>Homme</term><term>Microélectrode</term><term>Noyau gris central</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease, caused by the loss of dopaminergic nigrostriatal projections, is a debilitating neurodegenerative disease characterized by bradykinesia, rigidity, tremor and postural instability. The dopamine precursor levodopa (L-dopa) is the most effective treatment for the amelioration of Parkinson's disease signs and symptoms, but long-term administration can lead to disabling motor fluctuations and L-dopa -induced dyskinesias (LIDs). Studies in rat striatal slices have shown dopamine to be an essential component of activity-dependent synaptic plasticity at the input to the basal ganglia, but dopamine is also released from ventrally projecting dendrites of the substantia nigra pars compacta (SNc) on the substantia nigra pars reticulata (SNr), a major output structure of the basal ganglia. We characterized synaptic plasticity in the SNr using field potentials evoked with a nearby microelectrode (fEPs), in 18 Parkinson's disease patients undergoing implantation of deep brain stimulating (DBS) electrodes in the subthalamic nucleus (STN). High frequency stimulation (HFS-four trains of 2s at 100 Hz) in the SNr failed to induce a lasting change in test fEPs (1 Hz) amplitudes in patients OFF medication (decayed to baseline by 160s). Following oral L-dopa administration, HFS induced a potentiation of the fEP amplitudes (+29.3% of baseline at 160s following a plateau). Our findings suggest that extrastriatal dopamine modulates activity-dependent synaptic plasticity at basal ganglia output neurons. Dopamine medication state clearly impacts fEP amplitude, and the lasting nature of the increase is reminiscent of LTP-like changes, indicating that aberrant synaptic plasticity may play a role in the pathophysiology of Parkinson's disease.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0006-8950</s0></fA01><fA03 i2="1"><s0>Brain</s0></fA03><fA05><s2>132</s2></fA05><fA06><s3>p. 2</s3></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Levodopa enhances synaptic plasticity in the substantia nigra pars reticulata of Parkinson's disease patients</s1></fA08><fA11 i1="01" i2="1"><s1>PRESCOTT (I. A.)</s1></fA11><fA11 i1="02" i2="1"><s1>DOSTROVSKY (J. O.)</s1></fA11><fA11 i1="03" i2="1"><s1>MORO (E.)</s1></fA11><fA11 i1="04" i2="1"><s1>HODAIE (M.)</s1></fA11><fA11 i1="05" i2="1"><s1>LOZANO (A. M.)</s1></fA11><fA11 i1="06" i2="1"><s1>HUTCHISON (W. D.)</s1></fA11><fA14 i1="01"><s1>Department of Physiology, University of Toronto</s1><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>6 aut.</sZ></fA14><fA14 i1="02"><s1>Division of Neurosurgery, Department of Surgery, Toronto Western Research Institute and Krembil Neuroscience Centre</s1><s3>CAN</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></fA14><fA20><s1>309-318</s1></fA20><fA21><s1>2009</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>998</s2><s5>354000185402950040</s5></fA43><fA44><s0>0000</s0><s1>© 2009 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>1 p.1/4</s0></fA45><fA47 i1="01" i2="1"><s0>09-0108581</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Brain</s0></fA64><fA66 i1="01"><s0>GBR</s0></fA66><fC01 i1="01" l="ENG"><s0>Parkinson's disease, caused by the loss of dopaminergic nigrostriatal projections, is a debilitating neurodegenerative disease characterized by bradykinesia, rigidity, tremor and postural instability. The dopamine precursor levodopa (L-dopa) is the most effective treatment for the amelioration of Parkinson's disease signs and symptoms, but long-term administration can lead to disabling motor fluctuations and L-dopa -induced dyskinesias (LIDs). Studies in rat striatal slices have shown dopamine to be an essential component of activity-dependent synaptic plasticity at the input to the basal ganglia, but dopamine is also released from ventrally projecting dendrites of the substantia nigra pars compacta (SNc) on the substantia nigra pars reticulata (SNr), a major output structure of the basal ganglia. We characterized synaptic plasticity in the SNr using field potentials evoked with a nearby microelectrode (fEPs), in 18 Parkinson's disease patients undergoing implantation of deep brain stimulating (DBS) electrodes in the subthalamic nucleus (STN). High frequency stimulation (HFS-four trains of 2s at 100 Hz) in the SNr failed to induce a lasting change in test fEPs (1 Hz) amplitudes in patients OFF medication (decayed to baseline by 160s). Following oral L-dopa administration, HFS induced a potentiation of the fEP amplitudes (+29.3% of baseline at 160s following a plateau). Our findings suggest that extrastriatal dopamine modulates activity-dependent synaptic plasticity at basal ganglia output neurons. Dopamine medication state clearly impacts fEP amplitude, and the lasting nature of the increase is reminiscent of LTP-like changes, indicating that aberrant synaptic plasticity may play a role in the pathophysiology of Parkinson's disease.</s0></fC01><fC02 i1="01" i2="X"><s0>002B17</s0></fC02><fC02 i1="02" i2="X"><s0>002B17G</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Maladie de Parkinson</s0><s2>NM</s2><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Parkinson disease</s0><s2>NM</s2><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Parkinson enfermedad</s0><s2>NM</s2><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Pathologie du système nerveux</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Nervous system diseases</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Sistema nervioso patología</s0><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Lévodopa</s0><s2>NK</s2><s2>FR</s2><s5>09</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Levodopa</s0><s2>NK</s2><s2>FR</s2><s5>09</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Levodopa</s0><s2>NK</s2><s2>FR</s2><s5>09</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Plasticité synaptique</s0><s5>10</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Synaptic plasticity</s0><s5>10</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Plasticidad sináptica</s0><s5>10</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Locus niger</s0><s5>11</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Locus niger</s0><s5>11</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Locus níger</s0><s5>11</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Homme</s0><s5>12</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Human</s0><s5>12</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Hombre</s0><s5>12</s5></fC03><fC03 i1="07" i2="X" l="FRE"><s0>Microélectrode</s0><s5>13</s5></fC03><fC03 i1="07" i2="X" l="ENG"><s0>Microelectrode</s0><s5>13</s5></fC03><fC03 i1="07" i2="X" l="SPA"><s0>Microeléctrodo</s0><s5>13</s5></fC03><fC03 i1="08" i2="X" l="FRE"><s0>Noyau gris central</s0><s5>14</s5></fC03><fC03 i1="08" i2="X" l="ENG"><s0>Basal ganglion</s0><s5>14</s5></fC03><fC03 i1="08" i2="X" l="SPA"><s0>Núcleo basal</s0><s5>14</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Encéphale</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Encephalon</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Encéfalo</s0><s5>37</s5></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Système nerveux central</s0><s5>38</s5></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Central nervous system</s0><s5>38</s5></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Sistema nervioso central</s0><s5>38</s5></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0><s5>39</s5></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Cerebral disorder</s0><s5>39</s5></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Encéfalo patología</s0><s5>39</s5></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Syndrome extrapyramidal</s0><s5>40</s5></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0><s5>40</s5></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0><s5>40</s5></fC07><fC07 i1="05" i2="X" l="FRE"><s0>Maladie dégénérative</s0><s5>41</s5></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Degenerative disease</s0><s5>41</s5></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0><s5>41</s5></fC07><fC07 i1="06" i2="X" l="FRE"><s0>Pathologie du système nerveux central</s0><s5>42</s5></fC07><fC07 i1="06" i2="X" l="ENG"><s0>Central nervous system disease</s0><s5>42</s5></fC07><fC07 i1="06" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0><s5>42</s5></fC07><fN21><s1>075</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard><server><NO>PASCAL 09-0108581 INIST</NO><ET>Levodopa enhances synaptic plasticity in the substantia nigra pars reticulata of Parkinson's disease patients</ET><AU>PRESCOTT (I. A.); DOSTROVSKY (J. O.); MORO (E.); HODAIE (M.); LOZANO (A. M.); HUTCHISON (W. D.)</AU><AF>Department of Physiology, University of Toronto/Canada (1 aut., 2 aut., 6 aut.); Division of Neurosurgery, Department of Surgery, Toronto Western Research Institute and Krembil Neuroscience Centre/Canada (2 aut., 3 aut., 4 aut., 5 aut., 6 aut.)</AF><DT>Publication en série; Niveau analytique</DT><SO>Brain; ISSN 0006-8950; Royaume-Uni; Da. 2009; Vol. 132; No. p. 2; Pp. 309-318; Bibl. 1 p.1/4</SO><LA>Anglais</LA><EA>Parkinson's disease, caused by the loss of dopaminergic nigrostriatal projections, is a debilitating neurodegenerative disease characterized by bradykinesia, rigidity, tremor and postural instability. The dopamine precursor levodopa (L-dopa) is the most effective treatment for the amelioration of Parkinson's disease signs and symptoms, but long-term administration can lead to disabling motor fluctuations and L-dopa -induced dyskinesias (LIDs). Studies in rat striatal slices have shown dopamine to be an essential component of activity-dependent synaptic plasticity at the input to the basal ganglia, but dopamine is also released from ventrally projecting dendrites of the substantia nigra pars compacta (SNc) on the substantia nigra pars reticulata (SNr), a major output structure of the basal ganglia. We characterized synaptic plasticity in the SNr using field potentials evoked with a nearby microelectrode (fEPs), in 18 Parkinson's disease patients undergoing implantation of deep brain stimulating (DBS) electrodes in the subthalamic nucleus (STN). High frequency stimulation (HFS-four trains of 2s at 100 Hz) in the SNr failed to induce a lasting change in test fEPs (1 Hz) amplitudes in patients OFF medication (decayed to baseline by 160s). Following oral L-dopa administration, HFS induced a potentiation of the fEP amplitudes (+29.3% of baseline at 160s following a plateau). Our findings suggest that extrastriatal dopamine modulates activity-dependent synaptic plasticity at basal ganglia output neurons. Dopamine medication state clearly impacts fEP amplitude, and the lasting nature of the increase is reminiscent of LTP-like changes, indicating that aberrant synaptic plasticity may play a role in the pathophysiology of Parkinson's disease.</EA><CC>002B17; 002B17G</CC><FD>Maladie de Parkinson; Pathologie du système nerveux; Lévodopa; Plasticité synaptique; Locus niger; Homme; Microélectrode; Noyau gris central</FD><FG>Encéphale; Système nerveux central; Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du système nerveux central</FG><ED>Parkinson disease; Nervous system diseases; Levodopa; Synaptic plasticity; Locus niger; Human; Microelectrode; Basal ganglion</ED><EG>Encephalon; Central nervous system; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease</EG><SD>Parkinson enfermedad; Sistema nervioso patología; Levodopa; Plasticidad sináptica; Locus níger; Hombre; Microeléctrodo; Núcleo basal</SD><LO>INIST-998.354000185402950040</LO><ID>09-0108581</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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