Simultaneous Intrastriatal 6-Hydroxydopamine and Quinolinic Acid Injection: A Model of Early-Stage Striatonigral Degeneration

Ghorayeb, Imad; Puschban, Zoe; Fernagut, Pierre‐Olivier; Scherfler, Christoph; Rouland, Richard; Wenning, Gregor K.; Tison, François

doi:10.1006/exnr.2000.7535

Cited by 52 publications

(38 citation statements)

References 62 publications

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“…Thus, widespread striatal tissue destruction might interfere with our behavior studies, where our results likely reflect striatal tissue damage to a similar degree as nigral dopaminergic cell loss. Loss of nigrostriatal terminals likely account for the ipsilateral turning behavior observed following apomorphine administration, as the dopaminergic nerve terminals are lost and cannot be super-sensitive to stimulation by a DA agonist (396)(397)(398)(399)(400). This is supported by our qRT-PCR-results showing very low levels of D2 in the injected hemisphere for both genotypes.…”

Section: Mpp+ Model Of Pdsupporting

confidence: 68%

Cytoprotective effects of growth factors: BDNF more potent than GDNF in an organotypic culture model of Parkinson's disease

et al. 2011

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Section: Mpp+ Model Of Pdsupporting

confidence: 68%

Cytoprotective effects of growth factors: BDNF more potent than GDNF in an organotypic culture model of Parkinson's disease

et al. 2011

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“…Single-toxin-double-lesion approach 6-OHDA (MFB) then QA (striatum) (sequential) 45,46 QA (striatum) then 6-OHDA (MFB) (sequential) 46 QA ϩ 6-OHDA (striatum) (simultaneous) 47 3-NP (striatum) 48 strategy generated a reproducible symptomatology closer to human MSA-P/SND, i.e., L-dopa-unresponsive parkinsonism/dystonia correlated with striatal outflow pathway lesions and severe nigral degeneration. However, due to ethical considerations, time-consuming experiments, the need for a great number of animals due to a marked interindividual susceptibility to these mitochondrial toxins, the model strategy was switched to systemic MPTP ϩ 3-NP mouse models.…”

Section: Double-toxin-double-lesion Approachmentioning

confidence: 99%

Multiple system atrophy: An update

et al. 2003

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Multiple system atrophy (MSA) is a sporadic neurodegenerative disorder that usually manifests in the early sixth decade of life and progresses relentlessly with a mean survival of 9 years. Clinically, MSA is dominated by autonomic/urogenital failure, which may be associated with either levodopa (L-dopa) -unresponsive parkinsonism in 80% of cases (MSA-P subtype) or with cerebellar ataxia in 20% of cases (MSA-C subtype). Pathologically, MSA is characterized by a neuronal multisystem degeneration and abnormal glial cytoplasmic inclusions containing alpha-synuclein aggregates. Pharmacological treatment of motor features is disappointing except for a transient L-dopa response in a minority of MSA-P patients. In contrast, autonomic and urogenital features of MSA should be identified early on, because they can be treated effectively in many instances. Neuroprotective strategies are presently unavailable, however, two multicentre European trials have been launched to evaluate the effects of riluzole and human recombinant growth hormone on disease progression in MSA. Clearly, further randomised, controlled trials are required to identify effective symptomatic or neuroprotective agents in MSA. Several in vivo models have become available to allow a careful preselection of candidate agents. Several research groups have been formed in Europe (EMSA-SG, NNIPPS) and United States (NAMSA-SG), providing a framework for coordinated trial activity in MSA.

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“…QA is a tryptophan metabolite and a glutamate NMDA agonist with potent excitotoxic effects. Once injected into the striatum QA preferentially induces loss of medium spiny GABAergic neurons, that constitute 90% of the striatal neurons, while sparing most of the remaining interneurons (Figueredo-Cardenas et al, 1998;Foster et al, 1983;Ghorayeb et al, 2001;Stone 1993). This model was first developed by the group of Wenning et al (1996) that administered 6-OHDA into the left MFB of male Wistar rats, followed 3-4 weeks later by intrastriatal injection of QA into the ipsilateral striatum.…”

Section: Rodent Animal Modelsmentioning

confidence: 98%

Animal Models of Neurodegenerative Diseases

Ghorayeb

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Gaillard

et al. 2010

Neurochemical Mechanisms in Disease

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The use of animals as models of neurodegenerative disorders has allowed the determination of biological targets and biomarkers of several diseases, has yielded new therapeutical perspectives, and is essential before performing novel clinical assays. This review discusses the nature, use, and limits of animal models and how to obtain them for several neurodegenerative disorders such as multiple system atrophy, amyotrophic lateral sclerosis, and Huntington's disease, with a special emphasis on Parkinson's and Alzheimer's diseases. When possible, rodent, invertebrate and primate models are presented and discussed in relation to human disease. Finally, we highlight discrepancies between animal models and human neuropathology leading to question the pertinence of some of these findings to human disorders probably because of the wide spectrum of parameters defining a disease. Another point raised by these studies is the growing necessity to standardize the experimental procedures used to obtain an animal model, housing and breeding conditions, assessments of phenotypes investigated and, ultimately the interpretation of results obtained and their relevance to the pathology.

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Simultaneous Intrastriatal 6-Hydroxydopamine and Quinolinic Acid Injection: A Model of Early-Stage Striatonigral Degeneration

Cited by 52 publications

References 62 publications

Cytoprotective effects of growth factors: BDNF more potent than GDNF in an organotypic culture model of Parkinson's disease

Cytoprotective effects of growth factors: BDNF more potent than GDNF in an organotypic culture model of Parkinson's disease

Multiple system atrophy: An update

Animal Models of Neurodegenerative Diseases

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