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Dysfunction of the cortico-basal ganglia-cortical loop in a rat model of early parkinsonism is reversed by metabotropic glutamate receptor 5 antagonism.

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Title: Dysfunction of the cortico-basal ganglia-cortical loop in a rat model of early parkinsonism is reversed by metabotropic glutamate receptor 5 antagonism.
Authors: Oueslati, Abid (AUTHOR), Breysse, Nathalie (AUTHOR), Amalric, Marianne (AUTHOR), Kerkerian‐Le Goff, Lydia (AUTHOR), Salin, Pascal (AUTHOR)
Source: European Journal of Neuroscience. Dec2005, Vol. 22 Issue 11, p2765-2774. 10p. 5 Graphs.
Subjects: Akinetic mutism, Drug antagonism, Brain stem diseases, Movement disorders, Parkinson's disease, Drug interactions, Therapeutics
Abstract: This study examined the cellular correlates of the akinetic deficits produced in Wistar rats by discrete bilateral 6-hydroxydopamine (6-OHDA) striatal infusions in the dorsolateral striatum, mimicking the preferential denervation of the motor striatal territory in early symptomatic stage of Parkinson's disease (PD). Intraneuronal gene expression of cytochrome oxidase subunit I (COI), a metabolic index of neuronal activity, was increased in the subthalamic nucleus, substantia nigra pars reticulata and decreased in frontal cortical areas, but paradoxically unchanged in the striatum, globus pallidus, entopeduncular nucleus and ventrolateral thalamic nucleus. Neither preproenkephalin A nor preprotachykinin mRNA expression, markers of striatal projection neurons, were modified in the denervated striatal area despite 90% loss of dopamine (DA) terminals. Preproenkephalin A mRNA expression was however, decreased in the nondepleted striatal region, suggesting compensatory increase of dopamine tone from those spared areas. A chronic treatment with the metabotropic glutamate receptor 5 (mGluR5) antagonist 2-methyl-6-(phenylethylnyl)-pyridine (MPEP), which alleviated the akinetic disorders produced by the lesion, reversed the lesion-induced variations of COI gene expression, moderately increased this marker in the structures unaffected by the lesion and did not modify the striatal neuropeptides gene expression. These data suggest that the expression of akinetic deficits in early parkinsonism is associated with focused metabolic changes in the cortico-basal ganglia-cortical loop downstream of the striatum and pallidal complex. [ABSTRACT FROM AUTHOR]
Copyright of European Journal of Neuroscience is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Label: Title
  Group: Ti
  Data: Dysfunction of the cortico-basal ganglia-cortical loop in a rat model of early parkinsonism is reversed by metabotropic glutamate receptor 5 antagonism.
– Name: Author
  Label: Authors
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  Data: <searchLink fieldCode="AR" term="%22Oueslati%2C+Abid%22">Oueslati, Abid</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Breysse%2C+Nathalie%22">Breysse, Nathalie</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Amalric%2C+Marianne%22">Amalric, Marianne</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Kerkerian‐Le+Goff%2C+Lydia%22">Kerkerian‐Le Goff, Lydia</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Salin%2C+Pascal%22">Salin, Pascal</searchLink> (AUTHOR)
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  Data: <searchLink fieldCode="JN" term="%22European+Journal+of+Neuroscience%22">European Journal of Neuroscience</searchLink>. Dec2005, Vol. 22 Issue 11, p2765-2774. 10p. 5 Graphs.
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  Data: <searchLink fieldCode="DE" term="%22Akinetic+mutism%22">Akinetic mutism</searchLink><br /><searchLink fieldCode="DE" term="%22Drug+antagonism%22">Drug antagonism</searchLink><br /><searchLink fieldCode="DE" term="%22Brain+stem+diseases%22">Brain stem diseases</searchLink><br /><searchLink fieldCode="DE" term="%22Movement+disorders%22">Movement disorders</searchLink><br /><searchLink fieldCode="DE" term="%22Parkinson's+disease%22">Parkinson's disease</searchLink><br /><searchLink fieldCode="DE" term="%22Drug+interactions%22">Drug interactions</searchLink><br /><searchLink fieldCode="DE" term="%22Therapeutics%22">Therapeutics</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: This study examined the cellular correlates of the akinetic deficits produced in Wistar rats by discrete bilateral 6-hydroxydopamine (6-OHDA) striatal infusions in the dorsolateral striatum, mimicking the preferential denervation of the motor striatal territory in early symptomatic stage of Parkinson's disease (PD). Intraneuronal gene expression of cytochrome oxidase subunit I (COI), a metabolic index of neuronal activity, was increased in the subthalamic nucleus, substantia nigra pars reticulata and decreased in frontal cortical areas, but paradoxically unchanged in the striatum, globus pallidus, entopeduncular nucleus and ventrolateral thalamic nucleus. Neither preproenkephalin A nor preprotachykinin mRNA expression, markers of striatal projection neurons, were modified in the denervated striatal area despite 90% loss of dopamine (DA) terminals. Preproenkephalin A mRNA expression was however, decreased in the nondepleted striatal region, suggesting compensatory increase of dopamine tone from those spared areas. A chronic treatment with the metabotropic glutamate receptor 5 (mGluR5) antagonist 2-methyl-6-(phenylethylnyl)-pyridine (MPEP), which alleviated the akinetic disorders produced by the lesion, reversed the lesion-induced variations of COI gene expression, moderately increased this marker in the structures unaffected by the lesion and did not modify the striatal neuropeptides gene expression. These data suggest that the expression of akinetic deficits in early parkinsonism is associated with focused metabolic changes in the cortico-basal ganglia-cortical loop downstream of the striatum and pallidal complex. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
  Group: Ab
  Data: <i>Copyright of European Journal of Neuroscience is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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      – Type: doi
        Value: 10.1111/j.1460-9568.2005.04498.x
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      – Code: eng
        Text: English
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        StartPage: 2765
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      – SubjectFull: Akinetic mutism
        Type: general
      – SubjectFull: Drug antagonism
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      – SubjectFull: Brain stem diseases
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      – SubjectFull: Movement disorders
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      – SubjectFull: Parkinson's disease
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      – SubjectFull: Drug interactions
        Type: general
      – SubjectFull: Therapeutics
        Type: general
    Titles:
      – TitleFull: Dysfunction of the cortico-basal ganglia-cortical loop in a rat model of early parkinsonism is reversed by metabotropic glutamate receptor 5 antagonism.
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            NameFull: Oueslati, Abid
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            NameFull: Amalric, Marianne
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            NameFull: Kerkerian‐Le Goff, Lydia
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              Text: Dec2005
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              Y: 2005
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