Effect of subthalamic nucleus or entopeduncular nucleus lesion on levodopa-induced neurochemical changes within the basal ganglia and on levodopa-induced motor alterations in 6-hydroxydopamine-lesioned rats
Identifieur interne : 000D85 ( PascalFrancis/Checkpoint ); précédent : 000D84; suivant : 000D86Effect of subthalamic nucleus or entopeduncular nucleus lesion on levodopa-induced neurochemical changes within the basal ganglia and on levodopa-induced motor alterations in 6-hydroxydopamine-lesioned rats
Auteurs : Céline Perier [France] ; Concepcio Marin [Espagne] ; Anna Jimenez [Espagne] ; Mercè Bonastre [Espagne] ; Eduardo Tolosa [Espagne] ; Etienne C. Hirsch [France]Source :
- Journal of neurochemistry [ 0022-3042 ] ; 2003.
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- Pascal (Inist)
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Abstract
Inactivation of the subthalamic nucleus (STN) or the internal segment of the pallidum (GPi)/entopeduncular nucleus (EP) by deep brain stimulation or lesioning alleviates clinical manifestations of Parkinson's disease (PD) as well as reducing the side-effects of levodopa treatment. However, the effects of STN or entopeduncular nucleus (EP) lesion on levodopa-related motor fluctuations and on neurochemical changes induced by levodopa remain largely unknown. The effects of such lesions on levodopa-induced motor alterations were studied in 6-hydroxydopamine (6-OHDA)-lesioned rats and were assessed neurochemically by analyzing the functional activity of the basal ganglia nuclei, using the expression levels of the mRNAs coding for glutamic acid decarboxylase and cytochrome oxidase as molecular markers of neuronal activity. At the striatal level, preproenkephalin (PPE) mRNA levels were analyzed. We found in 6-OHDA-lesioned rats that a unilateral STN or EP lesion ipsilateral to the 6-OHDA lesion had no effect on either the shortening in the duration of the levodopa-induced rotational response or the levodopa-induced biochemical changes in the basal ganglia nuclei. In contrast, overexpression of PPE mRNA due to levodopa treatment was reversed by the STN or EP lesion. Our study thus shows that lesion of the EP or STN may counteract some of the neurochemical changes induced by levodopa treatment within the striatum.
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en" level="a">Effect of subthalamic nucleus or entopeduncular nucleus lesion on levodopa-induced neurochemical changes within the basal ganglia and on levodopa-induced motor alterations in 6-hydroxydopamine-lesioned rats</title><author><name sortKey="Perier, Celine" sort="Perier, Celine" uniqKey="Perier C" first="Céline" last="Perier">Céline Perier</name><affiliation wicri:level="3"><inist:fA14 i1="01"><s1>INSERM U289, Experimental Neurology and Therapeutics, Hopital de la Salpêtrière</s1><s2>Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Marin, Concepcio" sort="Marin, Concepcio" uniqKey="Marin C" first="Concepcio" last="Marin">Concepcio Marin</name><affiliation wicri:level="3"><inist:fA14 i1="02"><s1>Laboratori de Neurologia Experimental, Fundació Clinic, IDIBAPS, Hospital Clinic</s1><s2>Barcelona</s2><s3>ESP</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Espagne</country><placeName><settlement type="city">Barcelone</settlement><region nuts="2" type="region">Catalogne</region></placeName></affiliation></author><author><name sortKey="Jimenez, Anna" sort="Jimenez, Anna" uniqKey="Jimenez A" first="Anna" last="Jimenez">Anna Jimenez</name><affiliation wicri:level="3"><inist:fA14 i1="02"><s1>Laboratori de Neurologia Experimental, Fundació Clinic, IDIBAPS, Hospital Clinic</s1><s2>Barcelona</s2><s3>ESP</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Espagne</country><placeName><settlement type="city">Barcelone</settlement><region nuts="2" type="region">Catalogne</region></placeName></affiliation></author><author><name sortKey="Bonastre, Merce" sort="Bonastre, Merce" uniqKey="Bonastre M" first="Mercè" last="Bonastre">Mercè Bonastre</name><affiliation wicri:level="3"><inist:fA14 i1="02"><s1>Laboratori de Neurologia Experimental, Fundació Clinic, IDIBAPS, Hospital Clinic</s1><s2>Barcelona</s2><s3>ESP</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Espagne</country><placeName><settlement type="city">Barcelone</settlement><region nuts="2" type="region">Catalogne</region></placeName></affiliation></author><author><name sortKey="Tolosa, Eduardo" sort="Tolosa, Eduardo" uniqKey="Tolosa E" first="Eduardo" last="Tolosa">Eduardo Tolosa</name><affiliation wicri:level="3"><inist:fA14 i1="02"><s1>Laboratori de Neurologia Experimental, Fundació Clinic, IDIBAPS, Hospital Clinic</s1><s2>Barcelona</s2><s3>ESP</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Espagne</country><placeName><settlement type="city">Barcelone</settlement><region nuts="2" type="region">Catalogne</region></placeName></affiliation></author><author><name sortKey="Hirsch, Etienne C" sort="Hirsch, Etienne C" uniqKey="Hirsch E" first="Etienne C." last="Hirsch">Etienne C. 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Hirsch</name><affiliation wicri:level="3"><inist:fA14 i1="01"><s1>INSERM U289, Experimental Neurology and Therapeutics, Hopital de la Salpêtrière</s1><s2>Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author></analytic><series><title level="j" type="main">Journal of neurochemistry</title><title level="j" type="abbreviated">J. neurochem.</title><idno type="ISSN">0022-3042</idno><imprint><date when="2003">2003</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Journal of neurochemistry</title><title level="j" type="abbreviated">J. neurochem.</title><idno type="ISSN">0022-3042</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animal</term><term>Corpus striatum</term><term>Cytochrome-c oxidase</term><term>Entopedoncular nucleus</term><term>Gene expression</term><term>Glutamate decarboxylase</term><term>Lesion</term><term>Levodopa</term><term>Pallidum</term><term>Parkinson disease</term><term>Parkinsonism</term><term>Rat</term><term>Subthalamic nucleus</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Noyau sousthalamique</term><term>Lésion</term><term>Lévodopa</term><term>Noyau entopédonculaire</term><term>Pallidum</term><term>Corps strié</term><term>Parkinsonisme</term><term>Cytochrome-c oxidase</term><term>Glutamate decarboxylase</term><term>Parkinson maladie</term><term>Expression génique</term><term>Animal</term><term>Rat</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Inactivation of the subthalamic nucleus (STN) or the internal segment of the pallidum (GPi)/entopeduncular nucleus (EP) by deep brain stimulation or lesioning alleviates clinical manifestations of Parkinson's disease (PD) as well as reducing the side-effects of levodopa treatment. However, the effects of STN or entopeduncular nucleus (EP) lesion on levodopa-related motor fluctuations and on neurochemical changes induced by levodopa remain largely unknown. The effects of such lesions on levodopa-induced motor alterations were studied in 6-hydroxydopamine (6-OHDA)-lesioned rats and were assessed neurochemically by analyzing the functional activity of the basal ganglia nuclei, using the expression levels of the mRNAs coding for glutamic acid decarboxylase and cytochrome oxidase as molecular markers of neuronal activity. At the striatal level, preproenkephalin (PPE) mRNA levels were analyzed. We found in 6-OHDA-lesioned rats that a unilateral STN or EP lesion ipsilateral to the 6-OHDA lesion had no effect on either the shortening in the duration of the levodopa-induced rotational response or the levodopa-induced biochemical changes in the basal ganglia nuclei. In contrast, overexpression of PPE mRNA due to levodopa treatment was reversed by the STN or EP lesion. Our study thus shows that lesion of the EP or STN may counteract some of the neurochemical changes induced by levodopa treatment within the striatum.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0022-3042</s0></fA01><fA02 i1="01"><s0>JONRA9</s0></fA02><fA03 i2="1"><s0>J. neurochem.</s0></fA03><fA05><s2>86</s2></fA05><fA06><s2>6</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Effect of subthalamic nucleus or entopeduncular nucleus lesion on levodopa-induced neurochemical changes within the basal ganglia and on levodopa-induced motor alterations in 6-hydroxydopamine-lesioned rats</s1></fA08><fA11 i1="01" i2="1"><s1>PERIER (Céline)</s1></fA11><fA11 i1="02" i2="1"><s1>MARIN (Concepcio)</s1></fA11><fA11 i1="03" i2="1"><s1>JIMENEZ (Anna)</s1></fA11><fA11 i1="04" i2="1"><s1>BONASTRE (Mercè)</s1></fA11><fA11 i1="05" i2="1"><s1>TOLOSA (Eduardo)</s1></fA11><fA11 i1="06" i2="1"><s1>HIRSCH (Etienne C.)</s1></fA11><fA14 i1="01"><s1>INSERM U289, Experimental Neurology and Therapeutics, Hopital de la Salpêtrière</s1><s2>Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>6 aut.</sZ></fA14><fA14 i1="02"><s1>Laboratori de Neurologia Experimental, Fundació Clinic, IDIBAPS, Hospital Clinic</s1><s2>Barcelona</s2><s3>ESP</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></fA14><fA20><s1>1328-1337</s1></fA20><fA21><s1>2003</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>4037</s2><s5>354000112822590020</s5></fA43><fA44><s0>0000</s0><s1>© 2004 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>1 p.3/4</s0></fA45><fA47 i1="01" i2="1"><s0>04-0114913</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Journal of neurochemistry</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>Inactivation of the subthalamic nucleus (STN) or the internal segment of the pallidum (GPi)/entopeduncular nucleus (EP) by deep brain stimulation or lesioning alleviates clinical manifestations of Parkinson's disease (PD) as well as reducing the side-effects of levodopa treatment. However, the effects of STN or entopeduncular nucleus (EP) lesion on levodopa-related motor fluctuations and on neurochemical changes induced by levodopa remain largely unknown. The effects of such lesions on levodopa-induced motor alterations were studied in 6-hydroxydopamine (6-OHDA)-lesioned rats and were assessed neurochemically by analyzing the functional activity of the basal ganglia nuclei, using the expression levels of the mRNAs coding for glutamic acid decarboxylase and cytochrome oxidase as molecular markers of neuronal activity. At the striatal level, preproenkephalin (PPE) mRNA levels were analyzed. We found in 6-OHDA-lesioned rats that a unilateral STN or EP lesion ipsilateral to the 6-OHDA lesion had no effect on either the shortening in the duration of the levodopa-induced rotational response or the levodopa-induced biochemical changes in the basal ganglia nuclei. In contrast, overexpression of PPE mRNA due to levodopa treatment was reversed by the STN or EP lesion. 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l="ENG"><s0>Central nervous system disease</s0><s5>24</s5></fC07><fC07 i1="09" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0><s5>24</s5></fC07><fC07 i1="10" i2="X" l="FRE"><s0>Système nerveux pathologie</s0><s5>25</s5></fC07><fC07 i1="10" i2="X" l="ENG"><s0>Nervous system diseases</s0><s5>25</s5></fC07><fC07 i1="10" i2="X" l="SPA"><s0>Sistema nervioso patología</s0><s5>25</s5></fC07><fC07 i1="11" i2="X" l="FRE"><s0>Noyau gris central</s0><s5>35</s5></fC07><fC07 i1="11" i2="X" l="ENG"><s0>Basal ganglion</s0><s5>35</s5></fC07><fC07 i1="11" i2="X" l="SPA"><s0>Núcleo basal</s0><s5>35</s5></fC07><fC07 i1="12" i2="X" l="FRE"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="12" i2="X" l="ENG"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="12" i2="X" l="SPA"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="13" i2="X" l="FRE"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="13" i2="X" l="ENG"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="13" i2="X" l="SPA"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="14" i2="X" l="FRE"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="14" i2="X" l="ENG"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="14" i2="X" l="SPA"><s0>Vertebrata</s0><s2>NS</s2></fC07><fN21><s1>075</s1></fN21></pA></standard></inist><affiliations><list><country><li>Espagne</li><li>France</li></country><region><li>Catalogne</li><li>Île-de-France</li></region><settlement><li>Barcelone</li><li>Paris</li></settlement></list><tree><country name="France"><region name="Île-de-France"><name sortKey="Perier, Celine" sort="Perier, Celine" uniqKey="Perier C" first="Céline" last="Perier">Céline Perier</name></region><name sortKey="Hirsch, Etienne C" sort="Hirsch, Etienne C" uniqKey="Hirsch E" first="Etienne C." last="Hirsch">Etienne C. Hirsch</name></country><country name="Espagne"><region name="Catalogne"><name sortKey="Marin, Concepcio" sort="Marin, Concepcio" uniqKey="Marin C" first="Concepcio" last="Marin">Concepcio Marin</name></region><name sortKey="Bonastre, Merce" sort="Bonastre, Merce" uniqKey="Bonastre M" first="Mercè" last="Bonastre">Mercè Bonastre</name><name sortKey="Jimenez, Anna" sort="Jimenez, Anna" uniqKey="Jimenez A" first="Anna" last="Jimenez">Anna Jimenez</name><name sortKey="Tolosa, Eduardo" sort="Tolosa, Eduardo" uniqKey="Tolosa E" first="Eduardo" last="Tolosa">Eduardo Tolosa</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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