ParkinsonFranceV1, PascalFrancis, Curation, bibRecord, 000575

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 : 000575 ( PascalFrancis/Curation ); précédent : 000574; suivant : 000576

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

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.

RBID : Pascal:04-0114913

Descripteurs français

Pascal (Inist)
- Noyau sousthalamique, Lésion, Lévodopa, Noyau entopédonculaire, Pallidum, Corps strié, Parkinsonisme, Cytochrome-c oxidase, Glutamate decarboxylase, Parkinson maladie, Expression génique, Animal, Rat.

English descriptors

KwdEn :
- Animal, Corpus striatum, Cytochrome-c oxidase, Entopedoncular nucleus, Gene expression, Glutamate decarboxylase, Lesion, Levodopa, Pallidum, Parkinson disease, Parkinsonism, Rat, Subthalamic nucleus.

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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A11	`04`	`1`		`@1 BONASTRE (Mercè)`
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C01	`01`		`ENG`	@0 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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N21				`@1 075`

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Le document en format XML

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<term>Glutamate decarboxylase</term>
<term>Lesion</term>
<term>Levodopa</term>
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<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>
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<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. 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.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B17G</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Noyau sousthalamique</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Subthalamic nucleus</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Núcleo subtalámico</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Lésion</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Lesion</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Lesión</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Lévodopa</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Levodopa</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Levodopa</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Noyau entopédonculaire</s0>
<s5>05</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Entopedoncular nucleus</s0>
<s5>05</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Núcleo entopeduncular</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Pallidum</s0>
<s5>06</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Pallidum</s0>
<s5>06</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Pallidum</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Corps strié</s0>
<s5>08</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Corpus striatum</s0>
<s5>08</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Cuerpo estriado</s0>
<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Parkinsonisme</s0>
<s2>NM</s2>
<s5>09</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Parkinsonism</s0>
<s2>NM</s2>
<s5>09</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Parkinson síndrome</s0>
<s2>NM</s2>
<s5>09</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Cytochrome-c oxidase</s0>
<s2>FE</s2>
<s5>10</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Cytochrome-c oxidase</s0>
<s2>FE</s2>
<s5>10</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Cytochrome-c oxidase</s0>
<s2>FE</s2>
<s5>10</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Glutamate decarboxylase</s0>
<s2>FE</s2>
<s5>11</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Glutamate decarboxylase</s0>
<s2>FE</s2>
<s5>11</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Glutamate decarboxylase</s0>
<s2>FE</s2>
<s5>11</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Parkinson maladie</s0>
<s5>12</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s5>12</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s5>12</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Expression génique</s0>
<s5>13</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>Gene expression</s0>
<s5>13</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>Expresión genética</s0>
<s5>13</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE"><s0>Animal</s0>
<s5>14</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG"><s0>Animal</s0>
<s5>14</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA"><s0>Animal</s0>
<s5>14</s5>
</fC03>
<fC03 i1="13" i2="X" l="FRE"><s0>Rat</s0>
<s5>54</s5>
</fC03>
<fC03 i1="13" i2="X" l="ENG"><s0>Rat</s0>
<s5>54</s5>
</fC03>
<fC03 i1="13" i2="X" l="SPA"><s0>Rata</s0>
<s5>54</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Oxidoreductases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Oxidoreductases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Oxidoreductases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Enzima</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Carboxy-lyases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Carboxy-lyases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Carboxy-lyases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Carbon-carbon lyases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Carbon-carbon lyases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Carbon-carbon lyases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Lyases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Lyases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Lyases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>20</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>20</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>20</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0>
<s5>22</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>22</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>22</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>23</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>23</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>23</s5>
</fC07>
<fC07 i1="09" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0>
<s5>24</s5>
</fC07>
<fC07 i1="09" i2="X" 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>
</record>

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	La maladie de Parkinson en France (serveur d'exploration)
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La maladie de Parkinson en France (serveur d'exploration)

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

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

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