Complex motor disturbances in a sequential double lesion rat model of striatonigral degeneration (multiple system atrophy)
Identifieur interne : 001321 ( PascalFrancis/Corpus ); précédent : 001320; suivant : 001322Complex 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. WenningSource :
- Neuroscience [ 0306-4522 ] ; 2000.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
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.
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Format Inist (serveur)
NO : | PASCAL 00-0441811 INIST |
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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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<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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<fC03 i1="06" i2="X" l="SPA"><s0>Modelo animal</s0>
<s5>14</s5>
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<s5>54</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Rat</s0>
<s5>54</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Rata</s0>
<s5>54</s5>
</fC03>
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<s5>38</s5>
</fC07>
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<s5>38</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0>
<s5>39</s5>
</fC07>
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<s5>39</s5>
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<s5>39</s5>
</fC07>
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<s5>40</s5>
</fC07>
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<s5>40</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0>
<s5>41</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>41</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>42</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>42</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>42</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
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<server><NO>PASCAL 00-0441811 INIST</NO>
<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>
<CC>002B17G</CC>
<FD>Lésion; Dégénérescence; Voie nigrostriatale; Parkinson maladie; Atrophie multisystématisée; Modèle animal; Rat</FD>
<FG>Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Rodentia; Mammalia; Vertebrata</FG>
<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>
<SD>Lesión; Degeneración; Vía nigroestriatal; Parkinson enfermedad; Atrofia multisistematizada; Modelo animal; Rata</SD>
<LO>INIST-17194.354000090838590060</LO>
<ID>00-0441811</ID>
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