Intralaminar thalamic nuclei lesions: widespread impact on dopamine denervation-mediated cellular defects in the rat basal ganglia.
Identifieur interne : 000415 ( Ncbi/Merge ); précédent : 000414; suivant : 000416Intralaminar thalamic nuclei lesions: widespread impact on dopamine denervation-mediated cellular defects in the rat basal ganglia.
Auteurs : Jean-Jacques Bacci [France] ; Philippe Kachidian ; Lydia Kerkerian-Le Goff ; Pascal SalinSource :
- Journal of neuropathology and experimental neurology [ 0022-3069 ] ; 2004.
English descriptors
- KwdEn :
- Adrenergic Agents (pharmacology), Animals, Autoradiography, Basal Ganglia (drug effects), Basal Ganglia (metabolism), Basal Ganglia (pathology), Carrier Proteins (biosynthesis), Carrier Proteins (drug effects), Dopamine (metabolism), Female, Gene Expression (drug effects), Glutamate Decarboxylase (biosynthesis), Glutamate Decarboxylase (drug effects), Ibotenic Acid (pharmacology), Immunohistochemistry, In Situ Hybridization, Intralaminar Thalamic Nuclei (drug effects), Intralaminar Thalamic Nuclei (pathology), Isoenzymes (biosynthesis), Isoenzymes (drug effects), Membrane Transport Proteins, Neurons (drug effects), Neurons (metabolism), Neurons (pathology), Neuropeptides (biosynthesis), Neuropeptides (drug effects), Oxidopamine (pharmacology), Parkinsonian Disorders (chemically induced), Rats, Rats, Wistar, Substantia Nigra (pathology), Sympathectomy, Chemical, Vesicular Glutamate Transport Protein 2, Vesicular Transport Proteins.
- MESH :
- chemical , biosynthesis : Carrier Proteins, Glutamate Decarboxylase, Isoenzymes, Neuropeptides.
- chemical , drug effects : Carrier Proteins, Glutamate Decarboxylase, Isoenzymes, Neuropeptides.
- chemical , metabolism : Dopamine.
- chemical , pharmacology : Adrenergic Agents, Ibotenic Acid, Oxidopamine.
- chemically induced : Parkinsonian Disorders.
- drug effects : Basal Ganglia, Gene Expression, Intralaminar Thalamic Nuclei, Neurons.
- metabolism : Basal Ganglia, Neurons.
- pathology : Basal Ganglia, Intralaminar Thalamic Nuclei, Neurons, Substantia Nigra.
- Animals, Autoradiography, Female, Immunohistochemistry, In Situ Hybridization, Membrane Transport Proteins, Rats, Rats, Wistar, Sympathectomy, Chemical, Vesicular Glutamate Transport Protein 2, Vesicular Transport Proteins.
Abstract
Intralaminar thalamic nuclei represent a major site of non-dopaminergic degeneration in Parkinson disease, but the impact of this degeneration on the pathophysiological functioning of basal ganglia remains unknown. To address this issue, we compared the effects of 6-hydroxydopamine-induced lesions of nigral dopamine neurons alone or combined with ibotenate-induced lesions of intralaminar thalamic neurons on markers of neuronal metabolic activity in the rat basal ganglia using in situ hybridization histochemistry. Thalamic lesions prevented most of the dopamine denervation-induced changes (i.e. the increases in mRNA levels of enkephalin and GAD67 in the striatum, of GAD67 in the globus pallidus and entopeduncular nucleus, and of cytochrome oxidase subunit-I in the subthalamic nucleus), but did not affect the downregulation of striatal substance P and upregulation of GAD67 in the substantia nigra pars reticulata. We also provide immunohistochemical evidence that thalamic lesions markedly decreased striatal expression of the vesicular glutamate transporter vGluT2, confirming the association of this transporter with the thalamic projections to the basal ganglia. Altogether, these data reveal a major antagonistic influence of thalamic and dopaminergic afferents onto the basal ganglia and suggest that degeneration of thalamic neurons in Parkinson disease may represent an important factor counteracting expression of the defects associated with the dopamine denervation.
PubMed: 14748558
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pubmed:14748558Le document en format XML
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type="city">Marseille</settlement></placeName></affiliation></author><author><name sortKey="Kachidian, Philippe" sort="Kachidian, Philippe" uniqKey="Kachidian P" first="Philippe" last="Kachidian">Philippe Kachidian</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">Journal of neuropathology and experimental neurology</title><idno type="ISSN">0022-3069</idno><imprint><date when="2004" type="published">2004</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adrenergic Agents (pharmacology)</term><term>Animals</term><term>Autoradiography</term><term>Basal Ganglia (drug 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induced)</term><term>Rats</term><term>Rats, Wistar</term><term>Substantia Nigra (pathology)</term><term>Sympathectomy, Chemical</term><term>Vesicular Glutamate Transport Protein 2</term><term>Vesicular Transport Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Carrier Proteins</term><term>Glutamate Decarboxylase</term><term>Isoenzymes</term><term>Neuropeptides</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Carrier Proteins</term><term>Glutamate Decarboxylase</term><term>Isoenzymes</term><term>Neuropeptides</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Adrenergic Agents</term><term>Ibotenic Acid</term><term>Oxidopamine</term></keywords><keywords scheme="MESH" qualifier="chemically induced" 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type="abstract" xml:lang="en">Intralaminar thalamic nuclei represent a major site of non-dopaminergic degeneration in Parkinson disease, but the impact of this degeneration on the pathophysiological functioning of basal ganglia remains unknown. To address this issue, we compared the effects of 6-hydroxydopamine-induced lesions of nigral dopamine neurons alone or combined with ibotenate-induced lesions of intralaminar thalamic neurons on markers of neuronal metabolic activity in the rat basal ganglia using in situ hybridization histochemistry. Thalamic lesions prevented most of the dopamine denervation-induced changes (i.e. the increases in mRNA levels of enkephalin and GAD67 in the striatum, of GAD67 in the globus pallidus and entopeduncular nucleus, and of cytochrome oxidase subunit-I in the subthalamic nucleus), but did not affect the downregulation of striatal substance P and upregulation of GAD67 in the substantia nigra pars reticulata. We also provide immunohistochemical evidence that thalamic lesions markedly decreased striatal expression of the vesicular glutamate transporter vGluT2, confirming the association of this transporter with the thalamic projections to the basal ganglia. Altogether, these data reveal a major antagonistic influence of thalamic and dopaminergic afferents onto the basal ganglia and suggest that degeneration of thalamic neurons in Parkinson disease may represent an important factor counteracting expression of the defects associated with the dopamine denervation.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">14748558</PMID><DateCreated><Year>2004</Year><Month>01</Month><Day>29</Day></DateCreated><DateCompleted><Year>2004</Year><Month>03</Month><Day>10</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0022-3069</ISSN><JournalIssue CitedMedium="Print"><Volume>63</Volume><Issue>1</Issue><PubDate><Year>2004</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Journal of neuropathology and experimental neurology</Title><ISOAbbreviation>J. Neuropathol. Exp. 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Thalamic lesions prevented most of the dopamine denervation-induced changes (i.e. the increases in mRNA levels of enkephalin and GAD67 in the striatum, of GAD67 in the globus pallidus and entopeduncular nucleus, and of cytochrome oxidase subunit-I in the subthalamic nucleus), but did not affect the downregulation of striatal substance P and upregulation of GAD67 in the substantia nigra pars reticulata. We also provide immunohistochemical evidence that thalamic lesions markedly decreased striatal expression of the vesicular glutamate transporter vGluT2, confirming the association of this transporter with the thalamic projections to the basal ganglia. Altogether, these data reveal a major antagonistic influence of thalamic and dopaminergic afferents onto the basal ganglia and suggest that degeneration of thalamic neurons in Parkinson disease may represent an important factor counteracting expression of the defects associated with the dopamine denervation.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bacci</LastName><ForeName>Jean-Jacques</ForeName><Initials>JJ</Initials><AffiliationInfo><Affiliation>Laboratoire de Neurobiologie Cellulaire et Fonctionnelle, Centre National de la Recherche Scientifique, Marseille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kachidian</LastName><ForeName>Philippe</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Kerkerian-Le Goff</LastName><ForeName>Lydia</ForeName><Initials>L</Initials></Author><Author 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PubStatus="pubmed"><Year>2004</Year><Month>1</Month><Day>30</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2004</Year><Month>3</Month><Day>11</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2004</Year><Month>1</Month><Day>30</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">14748558</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>France</li></country><region><li>Provence-Alpes-Côte d'Azur</li></region><settlement><li>Marseille</li></settlement></list><tree><noCountry><name sortKey="Kachidian, Philippe" sort="Kachidian, Philippe" uniqKey="Kachidian P" first="Philippe" last="Kachidian">Philippe Kachidian</name><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><name sortKey="Salin, Pascal" sort="Salin, Pascal" uniqKey="Salin P" first="Pascal" last="Salin">Pascal Salin</name></noCountry><country name="France"><region name="Provence-Alpes-Côte d'Azur"><name sortKey="Bacci, Jean Jacques" sort="Bacci, Jean Jacques" uniqKey="Bacci J" first="Jean-Jacques" last="Bacci">Jean-Jacques Bacci</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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