Neuroprotective effect of chronic inactivation of the subthalamic nucleus in a rat model of Parkinson's disease.
Identifieur interne : 001434 ( PubMed/Corpus ); précédent : 001433; suivant : 001435Neuroprotective effect of chronic inactivation of the subthalamic nucleus in a rat model of Parkinson's disease.
Auteurs : B. Piallat ; A. Benazzouz ; A L BenabidSource :
- Journal of neural transmission. Supplementum [ 0303-6995 ] ; 1999.
English descriptors
- KwdEn :
- MESH :
- chemical , physiology : Dopamine.
- physiology : Behavior, Animal, Neurons, Thalamic Nuclei.
- therapy : Parkinson Disease, Secondary.
- Animals, Disease Models, Animal, Immunohistochemistry, Rats.
Abstract
Several evidences showed that glutamate can be implicated in the degenerative process of dopaminergic neurons in Parkinson's disease. The treatment with NMDA antagonists have been shown to induce a neuroprotective effect in animal models of this disease. As subthalamic nucleus neurons send direct glutamatergic projections to the substantia nigra, we studied the effects of kainic acid lesion of this nucleus on the degeneration of dopaminergic neurons induced by microinjection of 6-hydroxydopamine in the striatum of rat done one week after the first lesion. Animals were killed 15 days after the injection of 6-hydroxydopamine. Immunohistochemical study showed that lesion of the subthalamic nucleus can prevent the degeneration of substantia nigra dopaminergic somata when carried out one week prior to 6-hydroxydopamine injection in the striatum. Nevertheless neurochemical results showed that this lesion did not antagonize the striatal 6-hydroxydopamine-induced dopamine depletion in the striatum 15 days after 6-hydroxydopamine injection.
PubMed: 10335494
Links to Exploration step
pubmed:10335494Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Neuroprotective effect of chronic inactivation of the subthalamic nucleus in a rat model of Parkinson's disease.</title><author><name sortKey="Piallat, B" sort="Piallat, B" uniqKey="Piallat B" first="B" last="Piallat">B. Piallat</name><affiliation><nlm:affiliation>Laboratoire de Neurobiologie Préclinique, INSERM U.318, CHU, Grenoble, France.</nlm:affiliation></affiliation></author><author><name sortKey="Benazzouz, A" sort="Benazzouz, A" uniqKey="Benazzouz A" first="A" last="Benazzouz">A. Benazzouz</name></author><author><name sortKey="Benabid, A L" sort="Benabid, A L" uniqKey="Benabid A" first="A L" last="Benabid">A L Benabid</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1999">1999</date><idno type="RBID">pubmed:10335494</idno><idno type="pmid">10335494</idno><idno type="wicri:Area/PubMed/Corpus">001434</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001434</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Neuroprotective effect of chronic inactivation of the subthalamic nucleus in a rat model of Parkinson's disease.</title><author><name sortKey="Piallat, B" sort="Piallat, B" uniqKey="Piallat B" first="B" last="Piallat">B. Piallat</name><affiliation><nlm:affiliation>Laboratoire de Neurobiologie Préclinique, INSERM U.318, CHU, Grenoble, France.</nlm:affiliation></affiliation></author><author><name sortKey="Benazzouz, A" sort="Benazzouz, A" uniqKey="Benazzouz A" first="A" last="Benazzouz">A. Benazzouz</name></author><author><name sortKey="Benabid, A L" sort="Benabid, A L" uniqKey="Benabid A" first="A L" last="Benabid">A L Benabid</name></author></analytic><series><title level="j">Journal of neural transmission. Supplementum</title><idno type="ISSN">0303-6995</idno><imprint><date when="1999" type="published">1999</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Behavior, Animal (physiology)</term><term>Disease Models, Animal</term><term>Dopamine (physiology)</term><term>Immunohistochemistry</term><term>Neurons (physiology)</term><term>Parkinson Disease, Secondary (therapy)</term><term>Rats</term><term>Thalamic Nuclei (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Behavior, Animal</term><term>Neurons</term><term>Thalamic Nuclei</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Immunohistochemistry</term><term>Rats</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Several evidences showed that glutamate can be implicated in the degenerative process of dopaminergic neurons in Parkinson's disease. The treatment with NMDA antagonists have been shown to induce a neuroprotective effect in animal models of this disease. As subthalamic nucleus neurons send direct glutamatergic projections to the substantia nigra, we studied the effects of kainic acid lesion of this nucleus on the degeneration of dopaminergic neurons induced by microinjection of 6-hydroxydopamine in the striatum of rat done one week after the first lesion. Animals were killed 15 days after the injection of 6-hydroxydopamine. Immunohistochemical study showed that lesion of the subthalamic nucleus can prevent the degeneration of substantia nigra dopaminergic somata when carried out one week prior to 6-hydroxydopamine injection in the striatum. Nevertheless neurochemical results showed that this lesion did not antagonize the striatal 6-hydroxydopamine-induced dopamine depletion in the striatum 15 days after 6-hydroxydopamine injection.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">10335494</PMID><DateCreated><Year>1999</Year><Month>08</Month><Day>03</Day></DateCreated><DateCompleted><Year>1999</Year><Month>08</Month><Day>03</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0303-6995</ISSN><JournalIssue CitedMedium="Print"><Volume>55</Volume><PubDate><Year>1999</Year></PubDate></JournalIssue><Title>Journal of neural transmission. Supplementum</Title><ISOAbbreviation>J. Neural Transm. Suppl.</ISOAbbreviation></Journal><ArticleTitle>Neuroprotective effect of chronic inactivation of the subthalamic nucleus in a rat model of Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>71-7</MedlinePgn></Pagination><Abstract><AbstractText>Several evidences showed that glutamate can be implicated in the degenerative process of dopaminergic neurons in Parkinson's disease. The treatment with NMDA antagonists have been shown to induce a neuroprotective effect in animal models of this disease. As subthalamic nucleus neurons send direct glutamatergic projections to the substantia nigra, we studied the effects of kainic acid lesion of this nucleus on the degeneration of dopaminergic neurons induced by microinjection of 6-hydroxydopamine in the striatum of rat done one week after the first lesion. Animals were killed 15 days after the injection of 6-hydroxydopamine. Immunohistochemical study showed that lesion of the subthalamic nucleus can prevent the degeneration of substantia nigra dopaminergic somata when carried out one week prior to 6-hydroxydopamine injection in the striatum. Nevertheless neurochemical results showed that this lesion did not antagonize the striatal 6-hydroxydopamine-induced dopamine depletion in the striatum 15 days after 6-hydroxydopamine injection.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Piallat</LastName><ForeName>B</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Laboratoire de Neurobiologie Préclinique, INSERM U.318, CHU, Grenoble, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Benazzouz</LastName><ForeName>A</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Benabid</LastName><ForeName>A L</ForeName><Initials>AL</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Austria</Country><MedlineTA>J Neural Transm Suppl</MedlineTA><NlmUniqueID>0425126</NlmUniqueID><ISSNLinking>0303-6995</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001522" MajorTopicYN="N">Behavior, Animal</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004298" MajorTopicYN="N">Dopamine</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007150" MajorTopicYN="N">Immunohistochemistry</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010302" MajorTopicYN="N">Parkinson Disease, Secondary</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013787" MajorTopicYN="N">Thalamic Nuclei</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>21</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1999</Year><Month>5</Month><Day>21</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1999</Year><Month>5</Month><Day>21</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1999</Year><Month>5</Month><Day>21</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">10335494</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonFranceV1/Data/PubMed/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001434 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd -nk 001434 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= ParkinsonFranceV1
|flux= PubMed
|étape= Corpus
|type= RBID
|clé= pubmed:10335494
|texte= Neuroprotective effect of chronic inactivation of the subthalamic nucleus in a rat model of Parkinson's disease.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/RBID.i -Sk "pubmed:10335494" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd \
| NlmPubMed2Wicri -a ParkinsonFranceV1
| This area was generated with Dilib version V0.6.29. |  |