Dysfunction of the cortico-basal ganglia-cortical loop in a rat model of early parkinsonism is reversed by metabotropic glutamate receptor 5 antagonism.
Identifieur interne : 000F16 ( PubMed/Corpus ); précédent : 000F15; suivant : 000F17Dysfunction of the cortico-basal ganglia-cortical loop in a rat model of early parkinsonism is reversed by metabotropic glutamate receptor 5 antagonism.
Auteurs : Abid Oueslati ; Nathalie Breysse ; Marianne Amalric ; Lydia Kerkerian-Le Goff ; Pascal SalinSource :
- The European journal of neuroscience [ 0953-816X ] ; 2005.
English descriptors
- KwdEn :
- Animals, Basal Ganglia (physiopathology), Cerebral Cortex (physiopathology), Denervation, Dopamine Uptake Inhibitors, Electron Transport Complex IV (biosynthesis), Electron Transport Complex IV (genetics), Enkephalins (metabolism), Excitatory Amino Acid Antagonists (therapeutic use), In Situ Hybridization, Male, Mazindol, Neostriatum (metabolism), Nerve Net (physiology), Neurons (metabolism), Oxidopamine, Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (drug therapy), Parkinson Disease, Secondary (physiopathology), Protein Precursors (metabolism), RNA, Messenger (biosynthesis), Rats, Rats, Wistar, Receptor, Metabotropic Glutamate 5, Receptors, Metabotropic Glutamate (antagonists & inhibitors), Sympatholytics, Tachykinins (metabolism), Thalamus (physiology).
- MESH :
- chemical , antagonists & inhibitors : Receptors, Metabotropic Glutamate.
- chemical , biosynthesis : Electron Transport Complex IV, RNA, Messenger.
- chemical , genetics : Electron Transport Complex IV.
- chemical , metabolism : Enkephalins, Protein Precursors, Tachykinins.
- chemical , therapeutic use : Excitatory Amino Acid Antagonists.
- chemical : Dopamine Uptake Inhibitors, Mazindol, Oxidopamine, Receptor, Metabotropic Glutamate 5, Sympatholytics.
- chemically induced : Parkinson Disease, Secondary.
- drug therapy : Parkinson Disease, Secondary.
- metabolism : Neostriatum, Neurons.
- physiology : Nerve Net, Thalamus.
- physiopathology : Basal Ganglia, Cerebral Cortex, Parkinson Disease, Secondary.
- Animals, Denervation, In Situ Hybridization, Male, Rats, Rats, Wistar.
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.
DOI: 10.1111/j.1460-9568.2005.04498.x
PubMed: 16324110
Links to Exploration step
pubmed:16324110Le document en format XML
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Le Goff L" first="Lydia" last="Kerkerian-Le Goff">Lydia Kerkerian-Le Goff</name></author><author><name sortKey="Salin, Pascal" sort="Salin, Pascal" uniqKey="Salin P" first="Pascal" last="Salin">Pascal Salin</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2005">2005</date><idno type="RBID">pubmed:16324110</idno><idno type="pmid">16324110</idno><idno type="doi">10.1111/j.1460-9568.2005.04498.x</idno><idno type="wicri:Area/PubMed/Corpus">000F16</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000F16</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Dysfunction of the cortico-basal ganglia-cortical loop in a rat model of early parkinsonism is reversed by metabotropic glutamate receptor 5 antagonism.</title><author><name sortKey="Oueslati, Abid" sort="Oueslati, Abid" uniqKey="Oueslati A" first="Abid" last="Oueslati">Abid Oueslati</name><affiliation><nlm:affiliation>Interactions Cellulaires, Neurodégénérescence et Neuroplasticité, UMR 6186, CNRS-Université de la Méditerranée, 31 chemin Joseph Aiguier, 13402 Marseille Cedex 20, France.</nlm:affiliation></affiliation></author><author><name sortKey="Breysse, Nathalie" sort="Breysse, Nathalie" uniqKey="Breysse N" first="Nathalie" last="Breysse">Nathalie Breysse</name></author><author><name sortKey="Amalric, Marianne" sort="Amalric, Marianne" uniqKey="Amalric M" first="Marianne" last="Amalric">Marianne Amalric</name></author><author><name sortKey="Kerkerian Le Goff, Lydia" sort="Kerkerian Le Goff, Lydia" uniqKey="Kerkerian Le Goff L" first="Lydia" last="Kerkerian-Le Goff">Lydia Kerkerian-Le Goff</name></author><author><name sortKey="Salin, Pascal" sort="Salin, Pascal" uniqKey="Salin P" first="Pascal" last="Salin">Pascal Salin</name></author></analytic><series><title level="j">The European journal of neuroscience</title><idno 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use" xml:lang="en"><term>Excitatory Amino Acid Antagonists</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Dopamine Uptake Inhibitors</term><term>Mazindol</term><term>Oxidopamine</term><term>Receptor, Metabotropic Glutamate 5</term><term>Sympatholytics</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Neostriatum</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Nerve Net</term><term>Thalamus</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Basal Ganglia</term><term>Cerebral Cortex</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" 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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.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16324110</PMID><DateCreated><Year>2005</Year><Month>12</Month><Day>05</Day></DateCreated><DateCompleted><Year>2006</Year><Month>02</Month><Day>07</Day></DateCompleted><DateRevised><Year>2015</Year><Month>11</Month><Day>19</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0953-816X</ISSN><JournalIssue CitedMedium="Print"><Volume>22</Volume><Issue>11</Issue><PubDate><Year>2005</Year><Month>Dec</Month></PubDate></JournalIssue><Title>The European journal of neuroscience</Title><ISOAbbreviation>Eur. J. Neurosci.</ISOAbbreviation></Journal><ArticleTitle>Dysfunction of the cortico-basal ganglia-cortical loop in a rat model of early parkinsonism is reversed by metabotropic glutamate receptor 5 antagonism.</ArticleTitle><Pagination><MedlinePgn>2765-74</MedlinePgn></Pagination><Abstract><AbstractText>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. 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