La maladie de Parkinson au Canada (serveur d'exploration)

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Quinolinic acid lesion of the nigrostriatal pathway : effect on turning behaviour and protection by elevation of endogenous kynurenic acid in rattus norvegicus

Identifieur interne : 000D74 ( PascalFrancis/Corpus ); précédent : 000D73; suivant : 000D75

Quinolinic acid lesion of the nigrostriatal pathway : effect on turning behaviour and protection by elevation of endogenous kynurenic acid in rattus norvegicus

Auteurs : A. F. Miranda ; M. A. Sutton ; R. J. Beninger ; K. Jhamandas ; R. J. Boegman

Source :

RBID : Pascal:99-0210506

Descripteurs français

English descriptors

Abstract

Endogenous excitotoxins have been implicated in degeneration of nigral dopaminergic neurons in Parkinson's disease. It may be possible to reduce neurodegeneration by blocking the effects of these endogenous agents. The present study shows that contralateral turning seen following quinolinic acid-induced lesions of the nigrostriatal dopaminergic pathway was reversed by a treatment that increased brain levels of kynurenic acid, an endogenous excitatory amino acid antagonist. The treatment consisted of nicotinylalanine (5.6 nmol/5 μl i.c.v.), an inhibitor of kynureninase and kynurenine hydroxylase plus the precursor kynurenine (450 mg/kg i.p.) plus probenencid (200 mg/kg i.p.), an inhibitor of organic acid transport. Thus, neuroprotection by increasing brain kynurenic acid in vivo may be useful in retarding cell loss in Parkinson's and other neurodegenerative diseases involving excitotoxicity.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

pA  
A01 01  1    @0 0304-3940
A02 01      @0 NELED5
A03   1    @0 Neurosci. lett.
A05       @2 262
A06       @2 2
A08 01  1  ENG  @1 Quinolinic acid lesion of the nigrostriatal pathway : effect on turning behaviour and protection by elevation of endogenous kynurenic acid in rattus norvegicus
A11 01  1    @1 MIRANDA (A. F.)
A11 02  1    @1 SUTTON (M. A.)
A11 03  1    @1 BENINGER (R. J.)
A11 04  1    @1 JHAMANDAS (K.)
A11 05  1    @1 BOEGMAN (R. J.)
A14 01      @1 Department of Pharmacology and Toxicology, Queen's University @2 Kingston, Ontario, K7L 3N6 @3 CAN @Z 1 aut. @Z 4 aut. @Z 5 aut.
A14 02      @1 Department of Psychology, Queen's University @2 Kingston, Ontario, K7L 3N6 @3 CAN @Z 2 aut. @Z 3 aut.
A14 03      @1 Department of Psychiatry, Queen's University @2 Kingston, Ontario, K7L 3N6 @3 CAN @Z 3 aut.
A20       @1 81-84
A21       @1 1999
A23 01      @0 ENG
A43 01      @1 INIST @2 17240 @5 354000074775170030
A44       @0 0000 @1 © 1999 INIST-CNRS. All rights reserved.
A45       @0 16 ref.
A47 01  1    @0 99-0210506
A60       @1 P
A61       @0 A
A64 01  1    @0 Neuroscience letters
A66 01      @0 IRL
C01 01    ENG  @0 Endogenous excitotoxins have been implicated in degeneration of nigral dopaminergic neurons in Parkinson's disease. It may be possible to reduce neurodegeneration by blocking the effects of these endogenous agents. The present study shows that contralateral turning seen following quinolinic acid-induced lesions of the nigrostriatal dopaminergic pathway was reversed by a treatment that increased brain levels of kynurenic acid, an endogenous excitatory amino acid antagonist. The treatment consisted of nicotinylalanine (5.6 nmol/5 μl i.c.v.), an inhibitor of kynureninase and kynurenine hydroxylase plus the precursor kynurenine (450 mg/kg i.p.) plus probenencid (200 mg/kg i.p.), an inhibitor of organic acid transport. Thus, neuroprotection by increasing brain kynurenic acid in vivo may be useful in retarding cell loss in Parkinson's and other neurodegenerative diseases involving excitotoxicity.
C02 01  X    @0 002B02B10
C03 01  X  FRE  @0 Lésion @5 01
C03 01  X  ENG  @0 Lesion @5 01
C03 01  X  SPA  @0 Lesión @5 01
C03 02  X  FRE  @0 Voie nigrostriatale @5 02
C03 02  X  ENG  @0 Nigrostriatal pathway @5 02
C03 02  X  SPA  @0 Vía nigroestriatal @5 02
C03 03  X  FRE  @0 Comportement rotation @5 03
C03 03  X  ENG  @0 Rotation behavior @5 03
C03 03  X  SPA  @0 Comportamiento rotación @5 03
C03 04  X  FRE  @0 Neuroprotecteur @5 04
C03 04  X  ENG  @0 Neuroprotective agent @5 04
C03 04  X  SPA  @0 Neuroprotector @5 04
C03 05  X  FRE  @0 Parkinson maladie @5 10
C03 05  X  ENG  @0 Parkinson disease @5 10
C03 05  X  SPA  @0 Parkinson enfermedad @5 10
C03 06  X  FRE  @0 Animal @5 11
C03 06  X  ENG  @0 Animal @5 11
C03 06  X  SPA  @0 Animal @5 11
C03 07  X  FRE  @0 Rat @5 54
C03 07  X  ENG  @0 Rat @5 54
C03 07  X  SPA  @0 Rata @5 54
C03 08  X  FRE  @0 Cynurénique acide @4 INC @5 81
C07 01  X  FRE  @0 Encéphale @5 23
C07 01  X  ENG  @0 Brain (vertebrata) @5 23
C07 01  X  SPA  @0 Encéfalo @5 23
C07 02  X  FRE  @0 Système nerveux central @5 24
C07 02  X  ENG  @0 Central nervous system @5 24
C07 02  X  SPA  @0 Sistema nervioso central @5 24
C07 03  X  FRE  @0 Rodentia @2 NS
C07 03  X  ENG  @0 Rodentia @2 NS
C07 03  X  SPA  @0 Rodentia @2 NS
C07 04  X  FRE  @0 Mammalia @2 NS
C07 04  X  ENG  @0 Mammalia @2 NS
C07 04  X  SPA  @0 Mammalia @2 NS
C07 05  X  FRE  @0 Vertebrata @2 NS
C07 05  X  ENG  @0 Vertebrata @2 NS
C07 05  X  SPA  @0 Vertebrata @2 NS
N21       @1 130

Format Inist (serveur)

NO : PASCAL 99-0210506 INIST
ET : Quinolinic acid lesion of the nigrostriatal pathway : effect on turning behaviour and protection by elevation of endogenous kynurenic acid in rattus norvegicus
AU : MIRANDA (A. F.); SUTTON (M. A.); BENINGER (R. J.); JHAMANDAS (K.); BOEGMAN (R. J.)
AF : Department of Pharmacology and Toxicology, Queen's University/Kingston, Ontario, K7L 3N6/Canada (1 aut., 4 aut., 5 aut.); Department of Psychology, Queen's University/Kingston, Ontario, K7L 3N6/Canada (2 aut., 3 aut.); Department of Psychiatry, Queen's University/Kingston, Ontario, K7L 3N6/Canada (3 aut.)
DT : Publication en série; Niveau analytique
SO : Neuroscience letters; ISSN 0304-3940; Coden NELED5; Irlande; Da. 1999; Vol. 262; No. 2; Pp. 81-84; Bibl. 16 ref.
LA : Anglais
EA : Endogenous excitotoxins have been implicated in degeneration of nigral dopaminergic neurons in Parkinson's disease. It may be possible to reduce neurodegeneration by blocking the effects of these endogenous agents. The present study shows that contralateral turning seen following quinolinic acid-induced lesions of the nigrostriatal dopaminergic pathway was reversed by a treatment that increased brain levels of kynurenic acid, an endogenous excitatory amino acid antagonist. The treatment consisted of nicotinylalanine (5.6 nmol/5 μl i.c.v.), an inhibitor of kynureninase and kynurenine hydroxylase plus the precursor kynurenine (450 mg/kg i.p.) plus probenencid (200 mg/kg i.p.), an inhibitor of organic acid transport. Thus, neuroprotection by increasing brain kynurenic acid in vivo may be useful in retarding cell loss in Parkinson's and other neurodegenerative diseases involving excitotoxicity.
CC : 002B02B10
FD : Lésion; Voie nigrostriatale; Comportement rotation; Neuroprotecteur; Parkinson maladie; Animal; Rat; Cynurénique acide
FG : Encéphale; Système nerveux central; Rodentia; Mammalia; Vertebrata
ED : Lesion; Nigrostriatal pathway; Rotation behavior; Neuroprotective agent; Parkinson disease; Animal; Rat
EG : Brain (vertebrata); Central nervous system; Rodentia; Mammalia; Vertebrata
SD : Lesión; Vía nigroestriatal; Comportamiento rotación; Neuroprotector; Parkinson enfermedad; Animal; Rata
LO : INIST-17240.354000074775170030
ID : 99-0210506

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Pascal:99-0210506

Le document en format XML

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<div type="abstract" xml:lang="en">Endogenous excitotoxins have been implicated in degeneration of nigral dopaminergic neurons in Parkinson's disease. It may be possible to reduce neurodegeneration by blocking the effects of these endogenous agents. The present study shows that contralateral turning seen following quinolinic acid-induced lesions of the nigrostriatal dopaminergic pathway was reversed by a treatment that increased brain levels of kynurenic acid, an endogenous excitatory amino acid antagonist. The treatment consisted of nicotinylalanine (5.6 nmol/5 μl i.c.v.), an inhibitor of kynureninase and kynurenine hydroxylase plus the precursor kynurenine (450 mg/kg i.p.) plus probenencid (200 mg/kg i.p.), an inhibitor of organic acid transport. Thus, neuroprotection by increasing brain kynurenic acid in vivo may be useful in retarding cell loss in Parkinson's and other neurodegenerative diseases involving excitotoxicity.</div>
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<fC03 i1="08" i2="X" l="FRE">
<s0>Cynurénique acide</s0>
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<s5>81</s5>
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<s0>Encéphale</s0>
<s5>23</s5>
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<s5>23</s5>
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<s5>23</s5>
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<s5>24</s5>
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<s5>24</s5>
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<s0>Sistema nervioso central</s0>
<s5>24</s5>
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<s0>Rodentia</s0>
<s2>NS</s2>
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<fC07 i1="03" i2="X" l="ENG">
<s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fN21>
<s1>130</s1>
</fN21>
</pA>
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<NO>PASCAL 99-0210506 INIST</NO>
<ET>Quinolinic acid lesion of the nigrostriatal pathway : effect on turning behaviour and protection by elevation of endogenous kynurenic acid in rattus norvegicus</ET>
<AU>MIRANDA (A. F.); SUTTON (M. A.); BENINGER (R. J.); JHAMANDAS (K.); BOEGMAN (R. J.)</AU>
<AF>Department of Pharmacology and Toxicology, Queen's University/Kingston, Ontario, K7L 3N6/Canada (1 aut., 4 aut., 5 aut.); Department of Psychology, Queen's University/Kingston, Ontario, K7L 3N6/Canada (2 aut., 3 aut.); Department of Psychiatry, Queen's University/Kingston, Ontario, K7L 3N6/Canada (3 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Neuroscience letters; ISSN 0304-3940; Coden NELED5; Irlande; Da. 1999; Vol. 262; No. 2; Pp. 81-84; Bibl. 16 ref.</SO>
<LA>Anglais</LA>
<EA>Endogenous excitotoxins have been implicated in degeneration of nigral dopaminergic neurons in Parkinson's disease. It may be possible to reduce neurodegeneration by blocking the effects of these endogenous agents. The present study shows that contralateral turning seen following quinolinic acid-induced lesions of the nigrostriatal dopaminergic pathway was reversed by a treatment that increased brain levels of kynurenic acid, an endogenous excitatory amino acid antagonist. The treatment consisted of nicotinylalanine (5.6 nmol/5 μl i.c.v.), an inhibitor of kynureninase and kynurenine hydroxylase plus the precursor kynurenine (450 mg/kg i.p.) plus probenencid (200 mg/kg i.p.), an inhibitor of organic acid transport. Thus, neuroprotection by increasing brain kynurenic acid in vivo may be useful in retarding cell loss in Parkinson's and other neurodegenerative diseases involving excitotoxicity.</EA>
<CC>002B02B10</CC>
<FD>Lésion; Voie nigrostriatale; Comportement rotation; Neuroprotecteur; Parkinson maladie; Animal; Rat; Cynurénique acide</FD>
<FG>Encéphale; Système nerveux central; Rodentia; Mammalia; Vertebrata</FG>
<ED>Lesion; Nigrostriatal pathway; Rotation behavior; Neuroprotective agent; Parkinson disease; Animal; Rat</ED>
<EG>Brain (vertebrata); Central nervous system; Rodentia; Mammalia; Vertebrata</EG>
<SD>Lesión; Vía nigroestriatal; Comportamiento rotación; Neuroprotector; Parkinson enfermedad; Animal; Rata</SD>
<LO>INIST-17240.354000074775170030</LO>
<ID>99-0210506</ID>
</server>
</inist>
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