Differential gene expression induced by chronic levodopa treatment in the striatum of rats with lesions of the nigrostriatal system
Identifieur interne : 000D07 ( PascalFrancis/Corpus ); précédent : 000D06; suivant : 000D08Differential gene expression induced by chronic levodopa treatment in the striatum of rats with lesions of the nigrostriatal system
Auteurs : Juan E. Ferrario ; Irene R. E. Taravini ; Sophie Mourlevat ; Andrea Stefano ; Marina A. Delfino ; Rita Raisman-Vozari ; M. Gustavo Murer ; Merle Ruberg ; Oscar GershanikSource :
- Journal of neurochemistry [ 0022-3042 ] ; 2004.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
Levodopa, the major treatment for patients with Parkinson's disease, has been shown to induce a variety of compensatory effects, including facilitation of sprouting by dopaminergic neurons, in experimental animals with lesions leading to denervation of the striatum. To better understand the cellular and molecular environment where most of these compensatory changes take place, in particular elements that might contribute to the recovery of dopaminergic innervation, we have constructed a differential expression library enriched in transcripts from the striata of rats with lesions of the medial forebrain bundle treated with levodopa for 6 months. We have used this library to screen an expression array of rat genes representing the major cell functions, and have identified several that are involved in neurotrophic mechanisms and plasticity. We have confirmed the differential expression of selected transcripts by non-radioactive in situ hybridization, and report that the growth factor pleiotrophin, myelin basic protein and calmodulin are overexpressed in the denervated striatum of levodopa-treated rats.
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Format Inist (serveur)
NO : | PASCAL 05-0171106 INIST |
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ET : | Differential gene expression induced by chronic levodopa treatment in the striatum of rats with lesions of the nigrostriatal system |
AU : | FERRARIO (Juan E.); TARAVINI (Irene R. E.); MOURLEVAT (Sophie); STEFANO (Andrea); DELFINO (Marina A.); RAISMAN-VOZARI (Rita); MURER (M. Gustavo); RUBERG (Merle); GERSHANIK (Oscar) |
AF : | Instituto de Investigaciones Farmacológicas (ININFA), UBA-CONICET/Buenos Aires/Argentine (1 aut., 2 aut., 4 aut., 5 aut., 9 aut.); INSERM U289, Hôpital de la Salpêtrière/Paris/France (3 aut., 6 aut., 8 aut.); Departamento de Fisiología, Facultad de Medicina, Universidad de Buenos Aires/Buenos Aires/Argentine (7 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Journal of neurochemistry; ISSN 0022-3042; Coden JONRA9; Royaume-Uni; Da. 2004; Vol. 90; No. 6; Pp. 1348-1358; Bibl. 1 p.1/2 |
LA : | Anglais |
EA : | Levodopa, the major treatment for patients with Parkinson's disease, has been shown to induce a variety of compensatory effects, including facilitation of sprouting by dopaminergic neurons, in experimental animals with lesions leading to denervation of the striatum. To better understand the cellular and molecular environment where most of these compensatory changes take place, in particular elements that might contribute to the recovery of dopaminergic innervation, we have constructed a differential expression library enriched in transcripts from the striata of rats with lesions of the medial forebrain bundle treated with levodopa for 6 months. We have used this library to screen an expression array of rat genes representing the major cell functions, and have identified several that are involved in neurotrophic mechanisms and plasticity. We have confirmed the differential expression of selected transcripts by non-radioactive in situ hybridization, and report that the growth factor pleiotrophin, myelin basic protein and calmodulin are overexpressed in the denervated striatum of levodopa-treated rats. |
CC : | 002B02B06; 002B17A01 |
FD : | Expression génique; Chronique; Lévodopa; Corps strié; Lésion; Voie nigrostriatale; Calmoduline; Myéline; Parkinson maladie; Protéine basique; Plasticité; Antiparkinsonien; Animal; Rat |
FG : | Encéphale pathologie; Noyau gris central; Système nerveux central; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie; Système nerveux pathologie; Rodentia; Mammalia; Vertebrata |
ED : | Gene expression; Chronic; Levodopa; Corpus striatum; Lesion; Nigrostriatal pathway; Calmodulin; Myelin; Parkinson disease; Basic protein; Plasticity; Antiparkinson agent; Animal; Rat |
EG : | Cerebral disorder; Basal ganglion; Central nervous system; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Nervous system diseases; Rodentia; Mammalia; Vertebrata |
SD : | Expresión genética; Crónico; Levodopa; Cuerpo estriado; Lesión; Vía nigroestriatal; Calmodulina; Mielina; Parkinson enfermedad; Proteína básica; Plasticidad; Antiparkinsoniano; Animal; Rata |
LO : | INIST-4037.354000122216860080 |
ID : | 05-0171106 |
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Pascal:05-0171106Le document en format XML
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<series><title level="j" type="main">Journal of neurochemistry</title>
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<front><div type="abstract" xml:lang="en">Levodopa, the major treatment for patients with Parkinson's disease, has been shown to induce a variety of compensatory effects, including facilitation of sprouting by dopaminergic neurons, in experimental animals with lesions leading to denervation of the striatum. To better understand the cellular and molecular environment where most of these compensatory changes take place, in particular elements that might contribute to the recovery of dopaminergic innervation, we have constructed a differential expression library enriched in transcripts from the striata of rats with lesions of the medial forebrain bundle treated with levodopa for 6 months. We have used this library to screen an expression array of rat genes representing the major cell functions, and have identified several that are involved in neurotrophic mechanisms and plasticity. We have confirmed the differential expression of selected transcripts by non-radioactive in situ hybridization, and report that the growth factor pleiotrophin, myelin basic protein and calmodulin are overexpressed in the denervated striatum of levodopa-treated rats.</div>
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<s5>05</s5>
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<fC03 i1="06" i2="X" l="FRE"><s0>Voie nigrostriatale</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Nigrostriatal pathway</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Vía nigroestriatal</s0>
<s5>06</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Calmoduline</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Calmodulin</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Calmodulina</s0>
<s5>07</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Myéline</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Myelin</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Mielina</s0>
<s5>08</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Parkinson maladie</s0>
<s5>09</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s5>09</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s5>09</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Protéine basique</s0>
<s5>10</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>Basic protein</s0>
<s5>10</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Proteína básica</s0>
<s5>10</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Plasticité</s0>
<s5>11</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>Plasticity</s0>
<s5>11</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>Plasticidad</s0>
<s5>11</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE"><s0>Antiparkinsonien</s0>
<s5>13</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG"><s0>Antiparkinson agent</s0>
<s5>13</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA"><s0>Antiparkinsoniano</s0>
<s5>13</s5>
</fC03>
<fC03 i1="13" i2="X" l="FRE"><s0>Animal</s0>
<s5>14</s5>
</fC03>
<fC03 i1="13" i2="X" l="ENG"><s0>Animal</s0>
<s5>14</s5>
</fC03>
<fC03 i1="13" i2="X" l="SPA"><s0>Animal</s0>
<s5>14</s5>
</fC03>
<fC03 i1="14" i2="X" l="FRE"><s0>Rat</s0>
<s5>54</s5>
</fC03>
<fC03 i1="14" i2="X" l="ENG"><s0>Rat</s0>
<s5>54</s5>
</fC03>
<fC03 i1="14" i2="X" l="SPA"><s0>Rata</s0>
<s5>54</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>20</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>20</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>20</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Noyau gris central</s0>
<s5>21</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Basal ganglion</s0>
<s5>21</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Núcleo basal</s0>
<s5>21</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Système nerveux central</s0>
<s5>22</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Central nervous system</s0>
<s5>22</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Sistema nervioso central</s0>
<s5>22</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0>
<s5>23</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>23</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>23</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>24</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>24</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>24</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0>
<s5>25</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>25</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>25</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Système nerveux pathologie</s0>
<s5>26</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>26</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>26</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="09" i2="X" l="FRE"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="09" i2="X" l="ENG"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="09" i2="X" l="SPA"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="10" i2="X" l="FRE"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="10" i2="X" l="ENG"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="10" i2="X" l="SPA"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fN21><s1>115</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
<server><NO>PASCAL 05-0171106 INIST</NO>
<ET>Differential gene expression induced by chronic levodopa treatment in the striatum of rats with lesions of the nigrostriatal system</ET>
<AU>FERRARIO (Juan E.); TARAVINI (Irene R. E.); MOURLEVAT (Sophie); STEFANO (Andrea); DELFINO (Marina A.); RAISMAN-VOZARI (Rita); MURER (M. Gustavo); RUBERG (Merle); GERSHANIK (Oscar)</AU>
<AF>Instituto de Investigaciones Farmacológicas (ININFA), UBA-CONICET/Buenos Aires/Argentine (1 aut., 2 aut., 4 aut., 5 aut., 9 aut.); INSERM U289, Hôpital de la Salpêtrière/Paris/France (3 aut., 6 aut., 8 aut.); Departamento de Fisiología, Facultad de Medicina, Universidad de Buenos Aires/Buenos Aires/Argentine (7 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Journal of neurochemistry; ISSN 0022-3042; Coden JONRA9; Royaume-Uni; Da. 2004; Vol. 90; No. 6; Pp. 1348-1358; Bibl. 1 p.1/2</SO>
<LA>Anglais</LA>
<EA>Levodopa, the major treatment for patients with Parkinson's disease, has been shown to induce a variety of compensatory effects, including facilitation of sprouting by dopaminergic neurons, in experimental animals with lesions leading to denervation of the striatum. To better understand the cellular and molecular environment where most of these compensatory changes take place, in particular elements that might contribute to the recovery of dopaminergic innervation, we have constructed a differential expression library enriched in transcripts from the striata of rats with lesions of the medial forebrain bundle treated with levodopa for 6 months. We have used this library to screen an expression array of rat genes representing the major cell functions, and have identified several that are involved in neurotrophic mechanisms and plasticity. We have confirmed the differential expression of selected transcripts by non-radioactive in situ hybridization, and report that the growth factor pleiotrophin, myelin basic protein and calmodulin are overexpressed in the denervated striatum of levodopa-treated rats.</EA>
<CC>002B02B06; 002B17A01</CC>
<FD>Expression génique; Chronique; Lévodopa; Corps strié; Lésion; Voie nigrostriatale; Calmoduline; Myéline; Parkinson maladie; Protéine basique; Plasticité; Antiparkinsonien; Animal; Rat</FD>
<FG>Encéphale pathologie; Noyau gris central; Système nerveux central; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie; Système nerveux pathologie; Rodentia; Mammalia; Vertebrata</FG>
<ED>Gene expression; Chronic; Levodopa; Corpus striatum; Lesion; Nigrostriatal pathway; Calmodulin; Myelin; Parkinson disease; Basic protein; Plasticity; Antiparkinson agent; Animal; Rat</ED>
<EG>Cerebral disorder; Basal ganglion; Central nervous system; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Nervous system diseases; Rodentia; Mammalia; Vertebrata</EG>
<SD>Expresión genética; Crónico; Levodopa; Cuerpo estriado; Lesión; Vía nigroestriatal; Calmodulina; Mielina; Parkinson enfermedad; Proteína básica; Plasticidad; Antiparkinsoniano; Animal; Rata</SD>
<LO>INIST-4037.354000122216860080</LO>
<ID>05-0171106</ID>
</server>
</inist>
</record>
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