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 : 000D75Quinolinic 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. BoegmanSource :
- Neuroscience letters [ 0304-3940 ] ; 1999.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
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.
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Pour connaître la documentation sur le format Inist Standard.
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Format Inist (serveur)
NO : | PASCAL 99-0210506 INIST |
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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:99-0210506Le document en format XML
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<front><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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<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>
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<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>
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