In vivo models of multiple system atrophy
Identifieur interne : 003886 ( Main/Exploration ); précédent : 003885; suivant : 003887In vivo models of multiple system atrophy
Auteurs : Pierre-Olivier Fernagut [États-Unis] ; Imad Ghorayeb [France] ; Elsa Diguet [France] ; François Tison [France]Source :
- Movement Disorders [ 0885-3185 ] ; 2005-08.
English descriptors
- KwdEn :
- 3‐NP, Animals, Antiparkinson Agents (therapeutic use), Corpus Striatum (metabolism), Corpus Striatum (pathology), Levodopa (therapeutic use), MPTP, MPTP Poisoning (metabolism), MSA‐P, Macaca fascicularis, Mice, Multiple System Atrophy (genetics), Multiple System Atrophy (metabolism), Multiple System Atrophy (pathology), Oxidopamine (metabolism), Parkinsonian Disorders (drug therapy), Parkinsonian Disorders (genetics), Parkinsonian Disorders (pathology), Point Mutation (genetics), Rats, Substantia Nigra (metabolism), Substantia Nigra (pathology), alpha-Synuclein (genetics), alpha-Synuclein (metabolism), alpha‐synuclein, levodopa‐unresponsive parkinsonism, multiple system atrophy, pathophysiology.
- MESH :
- chemical , genetics : alpha-Synuclein.
- chemical , metabolism : Oxidopamine, alpha-Synuclein.
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- drug therapy : Parkinsonian Disorders.
- genetics : Multiple System Atrophy, Parkinsonian Disorders, Point Mutation.
- metabolism : Corpus Striatum, MPTP Poisoning, Multiple System Atrophy, Substantia Nigra.
- pathology : Corpus Striatum, Multiple System Atrophy, Parkinsonian Disorders, Substantia Nigra.
- Animals, Macaca fascicularis, Mice, Rats.
Abstract
Multiple system atrophy (MSA) is a sporadic adult‐onset neurodegenerative disorder of unknown etiology clinically characterized by a combination of parkinsonian, pyramidal, and cerebellar signs. Levodopa‐unresponsive parkinsonism is present in 80% of MSA cases, and this dominant clinical presentation (MSA‐P) is associated with a combined degeneration of the substantia nigra pars compacta and the striatum in anatomically related areas. The limited knowledge of the pathophysiology of MSA and the lack of therapeutic strategies prompted the development of lesion models reproducing striatonigral degeneration, the substrate of levodopa‐unresponsive parkinsonism in MSA‐P. This method was carried out first in rats with two different stereotaxic strategies using either two neurotoxins (“double toxin–double lesion”) or a single neurotoxin (“single toxin–double lesion”). Double‐lesioned rat models showed severe motor impairment compared to those with a single nigral or striatal lesion and helped to mimic different stages of the disease. Systemic models were also developed in mice and primates using the nigral toxin 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP) and the striatal toxin 3‐nitropropionic (3‐NP). In mice, although MPTP reduced the subsequent sensitivity to 3‐NP in a sequential lesion, simultaneous nigral and striatal insults were shown to exacerbate striatal damage. MPTP‐treated monkeys displayed a significant worsening of parkinsonism and a loss of levodopa‐responsiveness after the appearance of hindlimb dystonia and striatal lesion formation induced by subsequent 3‐NP intoxication. The different species and intoxication paradigms used will be useful to investigate functional changes in substantia nigra and striatum and to define neuroprotective, neurorestorative, or symptomatic therapeutic strategies. © 2005 Movement Disorder Society
Url:
DOI: 10.1002/mds.20541
Affiliations:
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<front><div type="abstract" xml:lang="en">Multiple system atrophy (MSA) is a sporadic adult‐onset neurodegenerative disorder of unknown etiology clinically characterized by a combination of parkinsonian, pyramidal, and cerebellar signs. Levodopa‐unresponsive parkinsonism is present in 80% of MSA cases, and this dominant clinical presentation (MSA‐P) is associated with a combined degeneration of the substantia nigra pars compacta and the striatum in anatomically related areas. The limited knowledge of the pathophysiology of MSA and the lack of therapeutic strategies prompted the development of lesion models reproducing striatonigral degeneration, the substrate of levodopa‐unresponsive parkinsonism in MSA‐P. This method was carried out first in rats with two different stereotaxic strategies using either two neurotoxins (“double toxin–double lesion”) or a single neurotoxin (“single toxin–double lesion”). Double‐lesioned rat models showed severe motor impairment compared to those with a single nigral or striatal lesion and helped to mimic different stages of the disease. Systemic models were also developed in mice and primates using the nigral toxin 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP) and the striatal toxin 3‐nitropropionic (3‐NP). In mice, although MPTP reduced the subsequent sensitivity to 3‐NP in a sequential lesion, simultaneous nigral and striatal insults were shown to exacerbate striatal damage. MPTP‐treated monkeys displayed a significant worsening of parkinsonism and a loss of levodopa‐responsiveness after the appearance of hindlimb dystonia and striatal lesion formation induced by subsequent 3‐NP intoxication. The different species and intoxication paradigms used will be useful to investigate functional changes in substantia nigra and striatum and to define neuroprotective, neurorestorative, or symptomatic therapeutic strategies. © 2005 Movement Disorder Society</div>
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