Comparative study of the effects of isatin, an endogenous MAO-inhibitor, and selegiline on bradykinesia and dopamine levels in a rat model of Parkinson's disease induced by the Japanese encephalitis virus
Identifieur interne : 000E40 ( PascalFrancis/Corpus ); précédent : 000E39; suivant : 000E41Comparative study of the effects of isatin, an endogenous MAO-inhibitor, and selegiline on bradykinesia and dopamine levels in a rat model of Parkinson's disease induced by the Japanese encephalitis virus
Auteurs : N. Hamaue ; M. Minami ; M. Terado ; M. Hirafuji ; T. Endo ; M. Machida ; T. Hiroshige ; A. Ogata ; K. Tashiro ; H. Saito ; S. H. ParvezSource :
- Neurotoxicology : (Park Forest South) [ 0161-813X ] ; 2004.
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English descriptors
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Abstract
We previously reported that exogenously administered isatin, an endogenous monoamine oxidase (MAO) inhibitor, significantly increased acetylcholine (ACh) and dopamine (DA) levels in the rat striatum. Selegiline [(-)-deprenil] was developed as a MAO-B inhibitor more than 30 years ago and widely used in the treatment of Parkinson's disease. Effects of isatin orselegiline were investigated in Japanese encephalitis virus (JEV)-induced post-encephalitic parkinsonism rats by a pole test for detecting motor activity and by the determination of biogenic amine levels. Motor activity of JEV-induced rats receiving isatin (100 mg/kg per day for 1 week, i.p.) or selegiline (0.2 mg/kg per day for I week, i.p.) was significantly improved compared with that of untreated JEV-infected rats. Both isatin and selegiline prevented the decrease in striatal DA levels in JEV-rats. The increased turnover of DA (DOPAC/DA) induced by JEV was significantly inhibited by isatin, but not by selegiline. These results suggested that exogenously administered isatin and selegiline can improve JEV-induced parkinsonism by increasing DA concentrations in the striatum.
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Format Inist (serveur)
| NO : | PASCAL 04-0194484 INIST |
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| ET : | Comparative study of the effects of isatin, an endogenous MAO-inhibitor, and selegiline on bradykinesia and dopamine levels in a rat model of Parkinson's disease induced by the Japanese encephalitis virus |
| AU : | HAMAUE (N.); MINAMI (M.); TERADO (M.); HIRAFUJI (M.); ENDO (T.); MACHIDA (M.); HIROSHIGE (T.); OGATA (A.); TASHIRO (K.); SAITO (H.); PARVEZ (S. H.); NICOTRA (A.); PARVEZ (S. H.); GLOVER (V.); SANDLER (M.); PARVEZ (S.); MINAMI (M.) |
| AF : | The Research Institute of Personalized Health Sciences, Health Sciences University of Hokkaido/061-0293 Ishikari-Tobetsu/Japon (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut.); Department of Neurology, Hokkaido University School of Medicine/060-8638 Sapporo/Japon (8 aut., 9 aut.); Department of Basic Sciences, Red-Cross Nursing College of Hokkaido/090-0011 Kitami, Hokkaido/Japon (10 aut.); Neuroendocrinology and Neuropharmacology, CNRS, Institute Alfred-Fessard-Bât 5/91190 Gif Sur Yvette/France (11 aut.); Dept. Animal and Human Biology, University of Rome I, Viale dell'Università 32/00198 Rome/Italie (1 aut.); Institut Alfred Fressard of Neuroscience, Bât5 Parc Chateau, CNRS/91190 Gif sur Yvette/France (2 aut., 5 aut.); Institute of Reproductive and Developmental Biology, Imperial College London, Hammersmith Campus, Du Cane Road/London, W12 ONN/Royaume-Uni (3 aut., 4 aut.); The Research Institute of Personalized Health, Health Sciences University of Hokkaido/061-0293 Ishikari-Tobetsu/Japon (6 aut.) |
| DT : | Publication en série; Niveau analytique |
| SO : | Neurotoxicology : (Park Forest South); ISSN 0161-813X; Etats-Unis; Da. 2004; Vol. 25; No. 1-2; Pp. 205-213; Bibl. 35 ref. |
| LA : | Anglais |
| EA : | We previously reported that exogenously administered isatin, an endogenous monoamine oxidase (MAO) inhibitor, significantly increased acetylcholine (ACh) and dopamine (DA) levels in the rat striatum. Selegiline [(-)-deprenil] was developed as a MAO-B inhibitor more than 30 years ago and widely used in the treatment of Parkinson's disease. Effects of isatin orselegiline were investigated in Japanese encephalitis virus (JEV)-induced post-encephalitic parkinsonism rats by a pole test for detecting motor activity and by the determination of biogenic amine levels. Motor activity of JEV-induced rats receiving isatin (100 mg/kg per day for 1 week, i.p.) or selegiline (0.2 mg/kg per day for I week, i.p.) was significantly improved compared with that of untreated JEV-infected rats. Both isatin and selegiline prevented the decrease in striatal DA levels in JEV-rats. The increased turnover of DA (DOPAC/DA) induced by JEV was significantly inhibited by isatin, but not by selegiline. These results suggested that exogenously administered isatin and selegiline can improve JEV-induced parkinsonism by increasing DA concentrations in the striatum. |
| CC : | 002A25; 002B03; 002B17 |
| FD : | Etude comparative; IMAO B; Amine oxidase (flavin-containing); Endogène; Inhibiteur enzyme; Catécholamine; Sélégiline; Stimulant dopaminergique; Parkinson maladie; Dopamine; Modèle animal; Encéphalite japonaise; Rat; Virus; Neurologie; Toxicologie |
| FG : | Oxidoreductases; Enzyme; Arbovirose; Virose; Infection; Rodentia; Mammalia; Vertebrata; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie; Système nerveux pathologie |
| ED : | Comparative study; MAO B inhibitor; Amine oxidase (flavin-containing); Endogenous; Enzyme inhibitor; Catecholamine; Selegiline; Dopamine agonist; Parkinson disease; Dopamine; Animal model; Japanese encephalitis; Rat; Virus; Neurology; Toxicology |
| EG : | Oxidoreductases; Enzyme; Arbovirus disease; Viral disease; Infection; Rodentia; Mammalia; Vertebrata; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Nervous system diseases |
| SD : | Estudio comparativo; IMOA B; Amine oxidase (flavin-containing); Endógeno; Inhibidor enzima; Catecolamina; Selegilina; Estimulante dopaminérgico; Parkinson enfermedad; Dopamina; Modelo animal; Encefalitis japonesa; Rata; Virus; Neurología; Toxicología |
| LO : | INIST-18397.354000119285470210 |
| ID : | 04-0194484 |
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Ogata</name><affiliation><inist:fA14 i1="02"><s1>Department of Neurology, Hokkaido University School of Medicine</s1><s2>060-8638 Sapporo</s2><s3>JPN</s3><sZ>8 aut.</sZ><sZ>9 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Tashiro, K" sort="Tashiro, K" uniqKey="Tashiro K" first="K." last="Tashiro">K. Tashiro</name><affiliation><inist:fA14 i1="02"><s1>Department of Neurology, Hokkaido University School of Medicine</s1><s2>060-8638 Sapporo</s2><s3>JPN</s3><sZ>8 aut.</sZ><sZ>9 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Saito, H" sort="Saito, H" uniqKey="Saito H" first="H." last="Saito">H. Saito</name><affiliation><inist:fA14 i1="03"><s1>Department of Basic Sciences, Red-Cross Nursing College of Hokkaido</s1><s2>090-0011 Kitami, Hokkaido</s2><s3>JPN</s3><sZ>10 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Parvez, S H" sort="Parvez, S H" uniqKey="Parvez S" first="S. H." last="Parvez">S. H. Parvez</name><affiliation><inist:fA14 i1="04"><s1>Neuroendocrinology and Neuropharmacology, CNRS, Institute Alfred-Fessard-Bât 5</s1><s2>91190 Gif Sur Yvette</s2><s3>FRA</s3><sZ>11 aut.</sZ></inist:fA14></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">04-0194484</idno><date when="2004">2004</date><idno type="stanalyst">PASCAL 04-0194484 INIST</idno><idno type="RBID">Pascal:04-0194484</idno><idno type="wicri:Area/PascalFrancis/Corpus">000E40</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Comparative study of the effects of isatin, an endogenous MAO-inhibitor, and selegiline on bradykinesia and dopamine levels in a rat model of Parkinson's disease induced by the Japanese encephalitis virus</title><author><name sortKey="Hamaue, N" sort="Hamaue, N" uniqKey="Hamaue N" first="N." last="Hamaue">N. Hamaue</name><affiliation><inist:fA14 i1="01"><s1>The Research Institute of Personalized Health Sciences, Health Sciences University of Hokkaido</s1><s2>061-0293 Ishikari-Tobetsu</s2><s3>JPN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Minami, M" sort="Minami, M" uniqKey="Minami M" first="M." last="Minami">M. Minami</name><affiliation><inist:fA14 i1="01"><s1>The Research Institute of Personalized Health Sciences, Health Sciences University of Hokkaido</s1><s2>061-0293 Ishikari-Tobetsu</s2><s3>JPN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Terado, M" sort="Terado, M" uniqKey="Terado M" first="M." last="Terado">M. Terado</name><affiliation><inist:fA14 i1="01"><s1>The Research Institute of Personalized Health Sciences, Health Sciences University of Hokkaido</s1><s2>061-0293 Ishikari-Tobetsu</s2><s3>JPN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Hirafuji, M" sort="Hirafuji, M" uniqKey="Hirafuji M" first="M." last="Hirafuji">M. Hirafuji</name><affiliation><inist:fA14 i1="01"><s1>The Research Institute of Personalized Health Sciences, Health Sciences University of Hokkaido</s1><s2>061-0293 Ishikari-Tobetsu</s2><s3>JPN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Endo, T" sort="Endo, T" uniqKey="Endo T" first="T." last="Endo">T. Endo</name><affiliation><inist:fA14 i1="01"><s1>The Research Institute of Personalized Health Sciences, Health Sciences University of Hokkaido</s1><s2>061-0293 Ishikari-Tobetsu</s2><s3>JPN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Machida, M" sort="Machida, M" uniqKey="Machida M" first="M." last="Machida">M. Machida</name><affiliation><inist:fA14 i1="01"><s1>The Research Institute of Personalized Health Sciences, Health Sciences University of Hokkaido</s1><s2>061-0293 Ishikari-Tobetsu</s2><s3>JPN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Hiroshige, T" sort="Hiroshige, T" uniqKey="Hiroshige T" first="T." last="Hiroshige">T. Hiroshige</name><affiliation><inist:fA14 i1="01"><s1>The Research Institute of Personalized Health Sciences, Health Sciences University of Hokkaido</s1><s2>061-0293 Ishikari-Tobetsu</s2><s3>JPN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Ogata, A" sort="Ogata, A" uniqKey="Ogata A" first="A." last="Ogata">A. Ogata</name><affiliation><inist:fA14 i1="02"><s1>Department of Neurology, Hokkaido University School of Medicine</s1><s2>060-8638 Sapporo</s2><s3>JPN</s3><sZ>8 aut.</sZ><sZ>9 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Tashiro, K" sort="Tashiro, K" uniqKey="Tashiro K" first="K." last="Tashiro">K. Tashiro</name><affiliation><inist:fA14 i1="02"><s1>Department of Neurology, Hokkaido University School of Medicine</s1><s2>060-8638 Sapporo</s2><s3>JPN</s3><sZ>8 aut.</sZ><sZ>9 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Saito, H" sort="Saito, H" uniqKey="Saito H" first="H." last="Saito">H. Saito</name><affiliation><inist:fA14 i1="03"><s1>Department of Basic Sciences, Red-Cross Nursing College of Hokkaido</s1><s2>090-0011 Kitami, Hokkaido</s2><s3>JPN</s3><sZ>10 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Parvez, S H" sort="Parvez, S H" uniqKey="Parvez S" first="S. H." last="Parvez">S. H. Parvez</name><affiliation><inist:fA14 i1="04"><s1>Neuroendocrinology and Neuropharmacology, CNRS, Institute Alfred-Fessard-Bât 5</s1><s2>91190 Gif Sur Yvette</s2><s3>FRA</s3><sZ>11 aut.</sZ></inist:fA14></affiliation></author></analytic><series><title level="j" type="main">Neurotoxicology : (Park Forest South)</title><title level="j" type="abbreviated">Neurotoxicology : (Park Forest South)</title><idno type="ISSN">0161-813X</idno><imprint><date when="2004">2004</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Neurotoxicology : (Park Forest South)</title><title level="j" type="abbreviated">Neurotoxicology : (Park Forest South)</title><idno type="ISSN">0161-813X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amine oxidase (flavin-containing)</term><term>Animal model</term><term>Catecholamine</term><term>Comparative study</term><term>Dopamine</term><term>Dopamine agonist</term><term>Endogenous</term><term>Enzyme inhibitor</term><term>Japanese encephalitis</term><term>MAO B inhibitor</term><term>Neurology</term><term>Parkinson disease</term><term>Rat</term><term>Selegiline</term><term>Toxicology</term><term>Virus</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Etude comparative</term><term>IMAO B</term><term>Amine oxidase (flavin-containing)</term><term>Endogène</term><term>Inhibiteur enzyme</term><term>Catécholamine</term><term>Sélégiline</term><term>Stimulant dopaminergique</term><term>Parkinson maladie</term><term>Dopamine</term><term>Modèle animal</term><term>Encéphalite japonaise</term><term>Rat</term><term>Virus</term><term>Neurologie</term><term>Toxicologie</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We previously reported that exogenously administered isatin, an endogenous monoamine oxidase (MAO) inhibitor, significantly increased acetylcholine (ACh) and dopamine (DA) levels in the rat striatum. Selegiline [(-)-deprenil] was developed as a MAO-B inhibitor more than 30 years ago and widely used in the treatment of Parkinson's disease. Effects of isatin orselegiline were investigated in Japanese encephalitis virus (JEV)-induced post-encephalitic parkinsonism rats by a pole test for detecting motor activity and by the determination of biogenic amine levels. Motor activity of JEV-induced rats receiving isatin (100 mg/kg per day for 1 week, i.p.) or selegiline (0.2 mg/kg per day for I week, i.p.) was significantly improved compared with that of untreated JEV-infected rats. Both isatin and selegiline prevented the decrease in striatal DA levels in JEV-rats. The increased turnover of DA (DOPAC/DA) induced by JEV was significantly inhibited by isatin, but not by selegiline. These results suggested that exogenously administered isatin and selegiline can improve JEV-induced parkinsonism by increasing DA concentrations in the striatum.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0161-813X</s0></fA01><fA03 i2="1"><s0>Neurotoxicology : (Park Forest South)</s0></fA03><fA05><s2>25</s2></fA05><fA06><s2>1-2</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Comparative study of the effects of isatin, an endogenous MAO-inhibitor, and selegiline on bradykinesia and dopamine levels in a rat model of Parkinson's disease induced by the Japanese encephalitis virus</s1></fA08><fA09 i1="01" i2="1" l="ENG"><s1>Monoamine Oxidases: Molecular, Pharmacological and Neurotoxicological Aspects. A Tribute to Prof. Merton Sandler</s1></fA09><fA11 i1="01" i2="1"><s1>HAMAUE (N.)</s1></fA11><fA11 i1="02" i2="1"><s1>MINAMI (M.)</s1></fA11><fA11 i1="03" i2="1"><s1>TERADO (M.)</s1></fA11><fA11 i1="04" i2="1"><s1>HIRAFUJI (M.)</s1></fA11><fA11 i1="05" i2="1"><s1>ENDO (T.)</s1></fA11><fA11 i1="06" i2="1"><s1>MACHIDA (M.)</s1></fA11><fA11 i1="07" i2="1"><s1>HIROSHIGE (T.)</s1></fA11><fA11 i1="08" i2="1"><s1>OGATA (A.)</s1></fA11><fA11 i1="09" i2="1"><s1>TASHIRO (K.)</s1></fA11><fA11 i1="10" i2="1"><s1>SAITO (H.)</s1></fA11><fA11 i1="11" i2="1"><s1>PARVEZ (S. H.)</s1></fA11><fA12 i1="01" i2="1"><s1>NICOTRA (A.)</s1><s9>ed.</s9></fA12><fA12 i1="02" i2="1"><s1>PARVEZ (S. H.)</s1><s9>ed.</s9></fA12><fA12 i1="03" i2="1"><s1>GLOVER (V.)</s1><s9>ed.</s9></fA12><fA12 i1="04" i2="1"><s1>SANDLER (M.)</s1><s9>ed.</s9></fA12><fA12 i1="05" i2="1"><s1>PARVEZ (S.)</s1><s9>ed.</s9></fA12><fA12 i1="06" i2="1"><s1>MINAMI (M.)</s1><s9>ed.</s9></fA12><fA14 i1="01"><s1>The Research Institute of Personalized Health Sciences, Health Sciences University of Hokkaido</s1><s2>061-0293 Ishikari-Tobetsu</s2><s3>JPN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ></fA14><fA14 i1="02"><s1>Department of Neurology, Hokkaido University School of Medicine</s1><s2>060-8638 Sapporo</s2><s3>JPN</s3><sZ>8 aut.</sZ><sZ>9 aut.</sZ></fA14><fA14 i1="03"><s1>Department of Basic Sciences, Red-Cross Nursing College of Hokkaido</s1><s2>090-0011 Kitami, Hokkaido</s2><s3>JPN</s3><sZ>10 aut.</sZ></fA14><fA14 i1="04"><s1>Neuroendocrinology and Neuropharmacology, CNRS, Institute Alfred-Fessard-Bât 5</s1><s2>91190 Gif Sur Yvette</s2><s3>FRA</s3><sZ>11 aut.</sZ></fA14><fA15 i1="01"><s1>Dept. Animal and Human Biology, University of Rome I, Viale dell'Università 32</s1><s2>00198 Rome</s2><s3>ITA</s3><sZ>1 aut.</sZ></fA15><fA15 i1="02"><s1>Institut Alfred Fressard of Neuroscience, Bât5 Parc Chateau, CNRS</s1><s2>91190 Gif sur Yvette</s2><s3>FRA</s3><sZ>2 aut.</sZ><sZ>5 aut.</sZ></fA15><fA15 i1="03"><s1>Institute of Reproductive and Developmental Biology, Imperial College London, Hammersmith Campus, Du Cane Road</s1><s2>London, W12 ONN</s2><s3>GBR</s3><sZ>3 aut.</sZ><sZ>4 aut.</sZ></fA15><fA15 i1="04"><s1>The Research Institute of Personalized Health, Health Sciences University of Hokkaido</s1><s2>061-0293 Ishikari-Tobetsu</s2><s3>JPN</s3><sZ>6 aut.</sZ></fA15><fA20><s1>205-213</s1></fA20><fA21><s1>2004</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>18397</s2><s5>354000119285470210</s5></fA43><fA44><s0>0000</s0><s1>© 2004 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>35 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>04-0194484</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Neurotoxicology : (Park Forest South)</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>We previously reported that exogenously administered isatin, an endogenous monoamine oxidase (MAO) inhibitor, significantly increased acetylcholine (ACh) and dopamine (DA) levels in the rat striatum. Selegiline [(-)-deprenil] was developed as a MAO-B inhibitor more than 30 years ago and widely used in the treatment of Parkinson's disease. Effects of isatin orselegiline were investigated in Japanese encephalitis virus (JEV)-induced post-encephalitic parkinsonism rats by a pole test for detecting motor activity and by the determination of biogenic amine levels. Motor activity of JEV-induced rats receiving isatin (100 mg/kg per day for 1 week, i.p.) or selegiline (0.2 mg/kg per day for I week, i.p.) was significantly improved compared with that of untreated JEV-infected rats. Both isatin and selegiline prevented the decrease in striatal DA levels in JEV-rats. The increased turnover of DA (DOPAC/DA) induced by JEV was significantly inhibited by isatin, but not by selegiline. These results suggested that exogenously administered isatin and selegiline can improve JEV-induced parkinsonism by increasing DA concentrations in the striatum.</s0></fC01><fC02 i1="01" i2="X"><s0>002A25</s0></fC02><fC02 i1="02" i2="X"><s0>002B03</s0></fC02><fC02 i1="03" i2="X"><s0>002B17</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Etude comparative</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Comparative study</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Estudio comparativo</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>IMAO B</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>MAO B inhibitor</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>IMOA B</s0><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Amine oxidase (flavin-containing)</s0><s2>FE</s2><s5>03</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Amine oxidase (flavin-containing)</s0><s2>FE</s2><s5>03</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Amine oxidase 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dégénérative</s0><s5>63</s5></fC07><fC07 i1="11" i2="X" l="ENG"><s0>Degenerative disease</s0><s5>63</s5></fC07><fC07 i1="11" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0><s5>63</s5></fC07><fC07 i1="12" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0><s5>64</s5></fC07><fC07 i1="12" i2="X" l="ENG"><s0>Central nervous system disease</s0><s5>64</s5></fC07><fC07 i1="12" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0><s5>64</s5></fC07><fC07 i1="13" i2="X" l="FRE"><s0>Système nerveux pathologie</s0><s5>65</s5></fC07><fC07 i1="13" i2="X" l="ENG"><s0>Nervous system diseases</s0><s5>65</s5></fC07><fC07 i1="13" i2="X" l="SPA"><s0>Sistema nervioso patología</s0><s5>65</s5></fC07><fN21><s1>131</s1></fN21><fN82><s1>OTO</s1></fN82></pA></standard><server><NO>PASCAL 04-0194484 INIST</NO><ET>Comparative study of the effects of isatin, an endogenous MAO-inhibitor, and selegiline on bradykinesia and dopamine levels in a rat model of Parkinson's disease induced by the Japanese encephalitis virus</ET><AU>HAMAUE (N.); MINAMI (M.); TERADO (M.); HIRAFUJI (M.); ENDO (T.); MACHIDA (M.); HIROSHIGE (T.); OGATA (A.); TASHIRO (K.); SAITO (H.); PARVEZ (S. H.); NICOTRA (A.); PARVEZ (S. H.); GLOVER (V.); SANDLER (M.); PARVEZ (S.); MINAMI (M.)</AU><AF>The Research Institute of Personalized Health Sciences, Health Sciences University of Hokkaido/061-0293 Ishikari-Tobetsu/Japon (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut.); Department of Neurology, Hokkaido University School of Medicine/060-8638 Sapporo/Japon (8 aut., 9 aut.); Department of Basic Sciences, Red-Cross Nursing College of Hokkaido/090-0011 Kitami, Hokkaido/Japon (10 aut.); Neuroendocrinology and Neuropharmacology, CNRS, Institute Alfred-Fessard-Bât 5/91190 Gif Sur Yvette/France (11 aut.); Dept. Animal and Human Biology, University of Rome I, Viale dell'Università 32/00198 Rome/Italie (1 aut.); Institut Alfred Fressard of Neuroscience, Bât5 Parc Chateau, CNRS/91190 Gif sur Yvette/France (2 aut., 5 aut.); Institute of Reproductive and Developmental Biology, Imperial College London, Hammersmith Campus, Du Cane Road/London, W12 ONN/Royaume-Uni (3 aut., 4 aut.); The Research Institute of Personalized Health, Health Sciences University of Hokkaido/061-0293 Ishikari-Tobetsu/Japon (6 aut.)</AF><DT>Publication en série; Niveau analytique</DT><SO>Neurotoxicology : (Park Forest South); ISSN 0161-813X; Etats-Unis; Da. 2004; Vol. 25; No. 1-2; Pp. 205-213; Bibl. 35 ref.</SO><LA>Anglais</LA><EA>We previously reported that exogenously administered isatin, an endogenous monoamine oxidase (MAO) inhibitor, significantly increased acetylcholine (ACh) and dopamine (DA) levels in the rat striatum. Selegiline [(-)-deprenil] was developed as a MAO-B inhibitor more than 30 years ago and widely used in the treatment of Parkinson's disease. Effects of isatin orselegiline were investigated in Japanese encephalitis virus (JEV)-induced post-encephalitic parkinsonism rats by a pole test for detecting motor activity and by the determination of biogenic amine levels. Motor activity of JEV-induced rats receiving isatin (100 mg/kg per day for 1 week, i.p.) or selegiline (0.2 mg/kg per day for I week, i.p.) was significantly improved compared with that of untreated JEV-infected rats. Both isatin and selegiline prevented the decrease in striatal DA levels in JEV-rats. The increased turnover of DA (DOPAC/DA) induced by JEV was significantly inhibited by isatin, but not by selegiline. These results suggested that exogenously administered isatin and selegiline can improve JEV-induced parkinsonism by increasing DA concentrations in the striatum.</EA><CC>002A25; 002B03; 002B17</CC><FD>Etude comparative; IMAO B; Amine oxidase (flavin-containing); Endogène; Inhibiteur enzyme; Catécholamine; Sélégiline; Stimulant dopaminergique; Parkinson maladie; Dopamine; Modèle animal; Encéphalite japonaise; Rat; Virus; Neurologie; Toxicologie</FD><FG>Oxidoreductases; Enzyme; Arbovirose; Virose; Infection; Rodentia; Mammalia; Vertebrata; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie; Système nerveux pathologie</FG><ED>Comparative study; MAO B inhibitor; Amine oxidase (flavin-containing); Endogenous; Enzyme inhibitor; Catecholamine; Selegiline; Dopamine agonist; Parkinson disease; Dopamine; Animal model; Japanese encephalitis; Rat; Virus; Neurology; Toxicology</ED><EG>Oxidoreductases; Enzyme; Arbovirus disease; Viral disease; Infection; Rodentia; Mammalia; Vertebrata; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Nervous system diseases</EG><SD>Estudio comparativo; IMOA B; Amine oxidase (flavin-containing); Endógeno; Inhibidor enzima; Catecolamina; Selegilina; Estimulante dopaminérgico; Parkinson enfermedad; Dopamina; Modelo animal; Encefalitis japonesa; Rata; Virus; Neurología; Toxicología</SD><LO>INIST-18397.354000119285470210</LO><ID>04-0194484</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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