ParkinsonFranceV1, PascalFrancis, Corpus, bibRecord, 001321

Complex motor disturbances in a sequential double lesion rat model of striatonigral degeneration (multiple system atrophy)

Identifieur interne : 001321 ( PascalFrancis/Corpus ); précédent : 001320; suivant : 001322

Complex motor disturbances in a sequential double lesion rat model of striatonigral degeneration (multiple system atrophy)

Auteurs : C. Scherfler ; Z. Puschban ; I. Ghorayeb ; G. P. Goebel ; F. Tison ; K. Jellinger ; W. Poewe ; G. K. Wenning

Source :

Neuroscience [ 0306-4522 ] ; 2000.

RBID : Pascal:00-0441811

Descripteurs français

Pascal (Inist)
- Lésion, Dégénérescence, Voie nigrostriatale, Parkinson maladie, Atrophie multisystématisée, Modèle animal, Rat.

English descriptors

KwdEn :
- Animal model, Degeneration, Lesion, Multiple system atrophy, Nigrostriatal pathway, Parkinson disease, Rat.

Abstract

This study characterizes paw reaching, stepping and balance abnormalities in a double lesion rat model of striatonigral degeneration, the core pathology underlying levodopa unresponsive parkinsonism associated with multiple system atrophy. Extensive unilateral nigral or striatal lesions induced by 6-hydroxydopamine or quinolinic acid, respectively, produced a similarly marked contralateral paw reaching deficit without further deterioration following a secondary (complementary) lesion of ipsilateral striatum or substantia nigra. Contralateral stepping rates were reduced by unilateral 6-hydroxydopamine lesions without further deterioration following the secondary striatal lesion. In contrast, initial unilateral striatal quinolinic acid injections induced bilateral stepping deficits that significantly worsened contralaterally following the secondary nigral lesion. Contralateral sidefalling rates were significantly increased following primary nigral and striatal lesions. Secondary nigral but not secondary striatal lesions worsened contralateral sidefalling rates. Histological studies revealed subtotal (>90%) depletion of dopaminergic neurons in substantia nigra pars compacta and variable degrees of striatal degeneration depending on the lesion sequence. Animals prelesioned with 6-hydroxydopamine showed significantly larger residual striatal surface areas following the secondary striatal quinolinic acid lesion compared to animals with primary striatal quinolinic acid lesions (P<0.001). These findings are in line with previous experimental studies demonstrating that striatal dopamine depletion confers neuroprotection against subsequent excitotoxic injury. Whether loss of dopaminergic neurons protects against the striatal disease process occurring in multiple system atrophy (Parkinson-type) remains to be elucidated. In summary, this is the first experimental study to investigate spontaneous motor behaviour in a unilateral double lesion rat model. Our observations are consistent with a complex interaction of nigral and striatal lesions producing distinct behavioural and histological changes depending on the lesion sequence. Tests of forelimb akinesia and complex motor behaviour appear to provide a reliable tool that will be helpful for monitoring the effects of interventional strategies such as embryonic neuronal transplantation in the rat model of striatonigral degeneration.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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C01	`01`		`ENG`	@0 This study characterizes paw reaching, stepping and balance abnormalities in a double lesion rat model of striatonigral degeneration, the core pathology underlying levodopa unresponsive parkinsonism associated with multiple system atrophy. Extensive unilateral nigral or striatal lesions induced by 6-hydroxydopamine or quinolinic acid, respectively, produced a similarly marked contralateral paw reaching deficit without further deterioration following a secondary (complementary) lesion of ipsilateral striatum or substantia nigra. Contralateral stepping rates were reduced by unilateral 6-hydroxydopamine lesions without further deterioration following the secondary striatal lesion. In contrast, initial unilateral striatal quinolinic acid injections induced bilateral stepping deficits that significantly worsened contralaterally following the secondary nigral lesion. Contralateral sidefalling rates were significantly increased following primary nigral and striatal lesions. Secondary nigral but not secondary striatal lesions worsened contralateral sidefalling rates. Histological studies revealed subtotal (>90%) depletion of dopaminergic neurons in substantia nigra pars compacta and variable degrees of striatal degeneration depending on the lesion sequence. Animals prelesioned with 6-hydroxydopamine showed significantly larger residual striatal surface areas following the secondary striatal quinolinic acid lesion compared to animals with primary striatal quinolinic acid lesions (P<0.001). These findings are in line with previous experimental studies demonstrating that striatal dopamine depletion confers neuroprotection against subsequent excitotoxic injury. Whether loss of dopaminergic neurons protects against the striatal disease process occurring in multiple system atrophy (Parkinson-type) remains to be elucidated. In summary, this is the first experimental study to investigate spontaneous motor behaviour in a unilateral double lesion rat model. Our observations are consistent with a complex interaction of nigral and striatal lesions producing distinct behavioural and histological changes depending on the lesion sequence. Tests of forelimb akinesia and complex motor behaviour appear to provide a reliable tool that will be helpful for monitoring the effects of interventional strategies such as embryonic neuronal transplantation in the rat model of striatonigral degeneration.
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C03	`03`	`X`	`FRE`	`@0 Voie nigrostriatale @5 04`
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Format Inist (serveur)

NO :	PASCAL 00-0441811 INIST
ET :	Complex motor disturbances in a sequential double lesion rat model of striatonigral degeneration (multiple system atrophy)
AU :	SCHERFLER (C.); PUSCHBAN (Z.); GHORAYEB (I.); GOEBEL (G. P.); TISON (F.); JELLINGER (K.); POEWE (W.); WENNING (G. K.)
AF :	Neurological Research Laboratory, University Hospital, Anichstrasse 35/6020 Innsbruck/Autriche (1 aut., 2 aut., 7 aut., 8 aut.); CNRS-UMR 5543, Université de Bordeaux 2, 146, rue Leo-Saignat/33076 Bordeaux/France (3 aut., 5 aut.); Institute of Biostatistics and Documentation, Schoepfstrasse 41/1/6020 Innsbruck/Autriche (4 aut.); Ludwig Boltzmann Institute for Clinical Neurobiology, Baumgartner Hoehe 1/1140 Vienna/Autriche (6 aut.)
DT :	Publication en série; Papier de recherche; Niveau analytique
SO :	Neuroscience; ISSN 0306-4522; Coden NRSCDN; Royaume-Uni; Da. 2000; Vol. 99; No. 1; Pp. 43-54; Bibl. 75 ref.
LA :	Anglais
EA :	This study characterizes paw reaching, stepping and balance abnormalities in a double lesion rat model of striatonigral degeneration, the core pathology underlying levodopa unresponsive parkinsonism associated with multiple system atrophy. Extensive unilateral nigral or striatal lesions induced by 6-hydroxydopamine or quinolinic acid, respectively, produced a similarly marked contralateral paw reaching deficit without further deterioration following a secondary (complementary) lesion of ipsilateral striatum or substantia nigra. Contralateral stepping rates were reduced by unilateral 6-hydroxydopamine lesions without further deterioration following the secondary striatal lesion. In contrast, initial unilateral striatal quinolinic acid injections induced bilateral stepping deficits that significantly worsened contralaterally following the secondary nigral lesion. Contralateral sidefalling rates were significantly increased following primary nigral and striatal lesions. Secondary nigral but not secondary striatal lesions worsened contralateral sidefalling rates. Histological studies revealed subtotal (>90%) depletion of dopaminergic neurons in substantia nigra pars compacta and variable degrees of striatal degeneration depending on the lesion sequence. Animals prelesioned with 6-hydroxydopamine showed significantly larger residual striatal surface areas following the secondary striatal quinolinic acid lesion compared to animals with primary striatal quinolinic acid lesions (P<0.001). These findings are in line with previous experimental studies demonstrating that striatal dopamine depletion confers neuroprotection against subsequent excitotoxic injury. Whether loss of dopaminergic neurons protects against the striatal disease process occurring in multiple system atrophy (Parkinson-type) remains to be elucidated. In summary, this is the first experimental study to investigate spontaneous motor behaviour in a unilateral double lesion rat model. Our observations are consistent with a complex interaction of nigral and striatal lesions producing distinct behavioural and histological changes depending on the lesion sequence. Tests of forelimb akinesia and complex motor behaviour appear to provide a reliable tool that will be helpful for monitoring the effects of interventional strategies such as embryonic neuronal transplantation in the rat model of striatonigral degeneration.
CC :	002B17G
FD :	Lésion; Dégénérescence; Voie nigrostriatale; Parkinson maladie; Atrophie multisystématisée; Modèle animal; Rat
FG :	Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Rodentia; Mammalia; Vertebrata
ED :	Lesion; Degeneration; Nigrostriatal pathway; Parkinson disease; Multiple system atrophy; Animal model; Rat
EG :	Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Rodentia; Mammalia; Vertebrata
SD :	Lesión; Degeneración; Vía nigroestriatal; Parkinson enfermedad; Atrofia multisistematizada; Modelo animal; Rata
LO :	INIST-17194.354000090838590060
ID :	00-0441811

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Pascal:00-0441811

Le document en format XML

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<front><div type="abstract" xml:lang="en">This study characterizes paw reaching, stepping and balance abnormalities in a double lesion rat model of striatonigral degeneration, the core pathology underlying levodopa unresponsive parkinsonism associated with multiple system atrophy. Extensive unilateral nigral or striatal lesions induced by 6-hydroxydopamine or quinolinic acid, respectively, produced a similarly marked contralateral paw reaching deficit without further deterioration following a secondary (complementary) lesion of ipsilateral striatum or substantia nigra. Contralateral stepping rates were reduced by unilateral 6-hydroxydopamine lesions without further deterioration following the secondary striatal lesion. In contrast, initial unilateral striatal quinolinic acid injections induced bilateral stepping deficits that significantly worsened contralaterally following the secondary nigral lesion. Contralateral sidefalling rates were significantly increased following primary nigral and striatal lesions. Secondary nigral but not secondary striatal lesions worsened contralateral sidefalling rates. Histological studies revealed subtotal (>90%) depletion of dopaminergic neurons in substantia nigra pars compacta and variable degrees of striatal degeneration depending on the lesion sequence. Animals prelesioned with 6-hydroxydopamine showed significantly larger residual striatal surface areas following the secondary striatal quinolinic acid lesion compared to animals with primary striatal quinolinic acid lesions (P<0.001). These findings are in line with previous experimental studies demonstrating that striatal dopamine depletion confers neuroprotection against subsequent excitotoxic injury. Whether loss of dopaminergic neurons protects against the striatal disease process occurring in multiple system atrophy (Parkinson-type) remains to be elucidated. In summary, this is the first experimental study to investigate spontaneous motor behaviour in a unilateral double lesion rat model. Our observations are consistent with a complex interaction of nigral and striatal lesions producing distinct behavioural and histological changes depending on the lesion sequence. Tests of forelimb akinesia and complex motor behaviour appear to provide a reliable tool that will be helpful for monitoring the effects of interventional strategies such as embryonic neuronal transplantation in the rat model of striatonigral degeneration.</div>
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<ET>Complex motor disturbances in a sequential double lesion rat model of striatonigral degeneration (multiple system atrophy)</ET>
<AU>SCHERFLER (C.); PUSCHBAN (Z.); GHORAYEB (I.); GOEBEL (G. P.); TISON (F.); JELLINGER (K.); POEWE (W.); WENNING (G. K.)</AU>
<AF>Neurological Research Laboratory, University Hospital, Anichstrasse 35/6020 Innsbruck/Autriche (1 aut., 2 aut., 7 aut., 8 aut.); CNRS-UMR 5543, Université de Bordeaux 2, 146, rue Leo-Saignat/33076 Bordeaux/France (3 aut., 5 aut.); Institute of Biostatistics and Documentation, Schoepfstrasse 41/1/6020 Innsbruck/Autriche (4 aut.); Ludwig Boltzmann Institute for Clinical Neurobiology, Baumgartner Hoehe 1/1140 Vienna/Autriche (6 aut.)</AF>
<DT>Publication en série; Papier de recherche; Niveau analytique</DT>
<SO>Neuroscience; ISSN 0306-4522; Coden NRSCDN; Royaume-Uni; Da. 2000; Vol. 99; No. 1; Pp. 43-54; Bibl. 75 ref.</SO>
<LA>Anglais</LA>
<EA>This study characterizes paw reaching, stepping and balance abnormalities in a double lesion rat model of striatonigral degeneration, the core pathology underlying levodopa unresponsive parkinsonism associated with multiple system atrophy. Extensive unilateral nigral or striatal lesions induced by 6-hydroxydopamine or quinolinic acid, respectively, produced a similarly marked contralateral paw reaching deficit without further deterioration following a secondary (complementary) lesion of ipsilateral striatum or substantia nigra. Contralateral stepping rates were reduced by unilateral 6-hydroxydopamine lesions without further deterioration following the secondary striatal lesion. In contrast, initial unilateral striatal quinolinic acid injections induced bilateral stepping deficits that significantly worsened contralaterally following the secondary nigral lesion. Contralateral sidefalling rates were significantly increased following primary nigral and striatal lesions. Secondary nigral but not secondary striatal lesions worsened contralateral sidefalling rates. Histological studies revealed subtotal (>90%) depletion of dopaminergic neurons in substantia nigra pars compacta and variable degrees of striatal degeneration depending on the lesion sequence. Animals prelesioned with 6-hydroxydopamine showed significantly larger residual striatal surface areas following the secondary striatal quinolinic acid lesion compared to animals with primary striatal quinolinic acid lesions (P<0.001). These findings are in line with previous experimental studies demonstrating that striatal dopamine depletion confers neuroprotection against subsequent excitotoxic injury. Whether loss of dopaminergic neurons protects against the striatal disease process occurring in multiple system atrophy (Parkinson-type) remains to be elucidated. In summary, this is the first experimental study to investigate spontaneous motor behaviour in a unilateral double lesion rat model. Our observations are consistent with a complex interaction of nigral and striatal lesions producing distinct behavioural and histological changes depending on the lesion sequence. Tests of forelimb akinesia and complex motor behaviour appear to provide a reliable tool that will be helpful for monitoring the effects of interventional strategies such as embryonic neuronal transplantation in the rat model of striatonigral degeneration.</EA>
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<ED>Lesion; Degeneration; Nigrostriatal pathway; Parkinson disease; Multiple system atrophy; Animal model; Rat</ED>
<EG>Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Rodentia; Mammalia; Vertebrata</EG>
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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)

Complex motor disturbances in a sequential double lesion rat model of striatonigral degeneration (multiple system atrophy)

Complex motor disturbances in a sequential double lesion rat model of striatonigral degeneration (multiple system atrophy)

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