Adaptive changes in the nigrostriatal pathway in response to increased 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurodegeneration in the mouse.
Identifieur interne : 001306 ( PubMed/Corpus ); précédent : 001305; suivant : 001307Adaptive changes in the nigrostriatal pathway in response to increased 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurodegeneration in the mouse.
Auteurs : E. Bezard ; M. Jaber ; F. Gonon ; A. Boireau ; B. Bloch ; C E GrossSource :
- The European journal of neuroscience [ 0953-816X ] ; 2000.
English descriptors
- KwdEn :
- 3,4-Dihydroxyphenylacetic Acid (metabolism), Animals, Carrier Proteins (metabolism), Cell Count, Corpus Striatum (metabolism), Corpus Striatum (pathology), Disease Models, Animal, Dopamine (pharmacokinetics), Dopamine Plasma Membrane Transport Proteins, Electric Stimulation, Electron Transport Complex IV (metabolism), Electrophysiology, Homovanillic Acid (metabolism), MPTP Poisoning (metabolism), MPTP Poisoning (pathology), Male, Membrane Glycoproteins, Membrane Transport Proteins, Mice, Mice, Inbred Strains, Nerve Degeneration (chemically induced), Nerve Degeneration (metabolism), Nerve Degeneration (pathology), Nerve Tissue Proteins, Neurons (enzymology), Neurons (pathology), Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (metabolism), Parkinson Disease, Secondary (pathology), Substantia Nigra (metabolism), Substantia Nigra (pathology), Synaptosomes (metabolism), Tritium, Tyrosine 3-Monooxygenase (analysis).
- MESH :
- chemical , analysis : Tyrosine 3-Monooxygenase.
- chemical , metabolism : 3,4-Dihydroxyphenylacetic Acid, Carrier Proteins, Electron Transport Complex IV, Homovanillic Acid.
- chemically induced : Nerve Degeneration, Parkinson Disease, Secondary.
- enzymology : Neurons.
- metabolism : Corpus Striatum, MPTP Poisoning, Nerve Degeneration, Parkinson Disease, Secondary, Substantia Nigra, Synaptosomes.
- pathology : Corpus Striatum, MPTP Poisoning, Nerve Degeneration, Neurons, Parkinson Disease, Secondary, Substantia Nigra.
- chemical , pharmacokinetics : Dopamine.
- Animals, Cell Count, Disease Models, Animal, Dopamine Plasma Membrane Transport Proteins, Electric Stimulation, Electrophysiology, Male, Membrane Glycoproteins, Membrane Transport Proteins, Mice, Mice, Inbred Strains, Nerve Tissue Proteins, Tritium.
Abstract
Although several adaptive mechanisms have been identified that mask the existence of Parkinson's disease and delay the onset and aggravation of motor symptoms, the timescale and implications of this compensatory process remain an enigma. In order to examine: (i) the nature of the dopaminergic adaptive mechanisms that come into action; (ii) their sequential activation in relation to the severity of degeneration; and (iii) their efficacy with regard to the maintenance of a normal level of basal ganglia activity, we analysed the brains of mice treated daily with 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine (MPTP, 4 mg/kg, i.p.) and killed at 5-day intervals from day 0 (D0) to D20. Our results demonstrate the sequential activation of two compensatory mechanisms: (i) an increase in striatal tyrosine hydroxylase (TH) protein content attested by the persistence of TH immunolabelling up to D15, contrasting with the decrease observed in both the number of nigral TH-immunoreactive neurons (-70.2%) and striatal dopamine content (-38.4%); (ii) a downregulation of DA uptake in surviving terminals at D20 (73.4% of nigral degeneration). At this point, the failure of adaptive mechanisms to maintain striatal dopaminergic homeostasis is also illustrated by an increase in the cytochrome oxidase activity of substantia nigra pars reticulata, a marker of neuronal function. It has been postulated that an increase in dopamine release per pulse could constitute an adaptive mechanism. The data we present from our MPTP mice model infirm this hypothesis. This study explores the link between the degree of nigral degeneration and the sequential activation of dopaminergic compensatory mechanisms in the nigrostriatal pathway and, in so doing, proposes a rethink of the paradigm applied to these mechanisms.
PubMed: 10971632
Links to Exploration step
pubmed:10971632Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Adaptive changes in the nigrostriatal pathway in response to increased 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurodegeneration in the mouse.</title><author><name sortKey="Bezard, E" sort="Bezard, E" uniqKey="Bezard E" first="E" last="Bezard">E. Bezard</name><affiliation><nlm:affiliation>Basal Gang, Laboratoire de Neurophysiologie, CNRS UMR 5543, Université Victor Segalen, 146 rue Léo Saignat, 33076 Bordeaux Cedex, France. erwan.bezard@umr5543.u-bordeaux2.fr</nlm:affiliation></affiliation></author><author><name sortKey="Jaber, M" sort="Jaber, M" uniqKey="Jaber M" first="M" last="Jaber">M. Jaber</name></author><author><name sortKey="Gonon, F" sort="Gonon, F" uniqKey="Gonon F" first="F" last="Gonon">F. Gonon</name></author><author><name sortKey="Boireau, A" sort="Boireau, A" uniqKey="Boireau A" first="A" last="Boireau">A. Boireau</name></author><author><name sortKey="Bloch, B" sort="Bloch, B" uniqKey="Bloch B" first="B" last="Bloch">B. Bloch</name></author><author><name sortKey="Gross, C E" sort="Gross, C E" uniqKey="Gross C" first="C E" last="Gross">C E Gross</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2000">2000</date><idno type="RBID">pubmed:10971632</idno><idno type="pmid">10971632</idno><idno type="wicri:Area/PubMed/Corpus">001306</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001306</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Adaptive changes in the nigrostriatal pathway in response to increased 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurodegeneration in the mouse.</title><author><name sortKey="Bezard, E" sort="Bezard, E" uniqKey="Bezard E" first="E" last="Bezard">E. Bezard</name><affiliation><nlm:affiliation>Basal Gang, Laboratoire de Neurophysiologie, CNRS UMR 5543, Université Victor Segalen, 146 rue Léo Saignat, 33076 Bordeaux Cedex, France. erwan.bezard@umr5543.u-bordeaux2.fr</nlm:affiliation></affiliation></author><author><name sortKey="Jaber, M" sort="Jaber, M" uniqKey="Jaber M" first="M" last="Jaber">M. Jaber</name></author><author><name sortKey="Gonon, F" sort="Gonon, F" uniqKey="Gonon F" first="F" last="Gonon">F. Gonon</name></author><author><name sortKey="Boireau, A" sort="Boireau, A" uniqKey="Boireau A" first="A" last="Boireau">A. Boireau</name></author><author><name sortKey="Bloch, B" sort="Bloch, B" uniqKey="Bloch B" first="B" last="Bloch">B. Bloch</name></author><author><name sortKey="Gross, C E" sort="Gross, C E" uniqKey="Gross C" first="C E" last="Gross">C E Gross</name></author></analytic><series><title level="j">The European journal of neuroscience</title><idno type="ISSN">0953-816X</idno><imprint><date when="2000" type="published">2000</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>3,4-Dihydroxyphenylacetic Acid (metabolism)</term><term>Animals</term><term>Carrier Proteins (metabolism)</term><term>Cell Count</term><term>Corpus Striatum (metabolism)</term><term>Corpus Striatum (pathology)</term><term>Disease Models, Animal</term><term>Dopamine (pharmacokinetics)</term><term>Dopamine Plasma Membrane Transport Proteins</term><term>Electric Stimulation</term><term>Electron Transport Complex IV (metabolism)</term><term>Electrophysiology</term><term>Homovanillic Acid (metabolism)</term><term>MPTP Poisoning (metabolism)</term><term>MPTP Poisoning (pathology)</term><term>Male</term><term>Membrane Glycoproteins</term><term>Membrane Transport Proteins</term><term>Mice</term><term>Mice, Inbred Strains</term><term>Nerve Degeneration (chemically induced)</term><term>Nerve Degeneration (metabolism)</term><term>Nerve Degeneration (pathology)</term><term>Nerve Tissue Proteins</term><term>Neurons (enzymology)</term><term>Neurons (pathology)</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson Disease, Secondary (metabolism)</term><term>Parkinson Disease, Secondary (pathology)</term><term>Substantia Nigra (metabolism)</term><term>Substantia Nigra (pathology)</term><term>Synaptosomes (metabolism)</term><term>Tritium</term><term>Tyrosine 3-Monooxygenase (analysis)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Tyrosine 3-Monooxygenase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>3,4-Dihydroxyphenylacetic Acid</term><term>Carrier Proteins</term><term>Electron Transport Complex IV</term><term>Homovanillic Acid</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Nerve Degeneration</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Corpus Striatum</term><term>MPTP Poisoning</term><term>Nerve Degeneration</term><term>Parkinson Disease, Secondary</term><term>Substantia Nigra</term><term>Synaptosomes</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Corpus Striatum</term><term>MPTP Poisoning</term><term>Nerve Degeneration</term><term>Neurons</term><term>Parkinson Disease, Secondary</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacokinetics" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Count</term><term>Disease Models, Animal</term><term>Dopamine Plasma Membrane Transport Proteins</term><term>Electric Stimulation</term><term>Electrophysiology</term><term>Male</term><term>Membrane Glycoproteins</term><term>Membrane Transport Proteins</term><term>Mice</term><term>Mice, Inbred Strains</term><term>Nerve Tissue Proteins</term><term>Tritium</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Although several adaptive mechanisms have been identified that mask the existence of Parkinson's disease and delay the onset and aggravation of motor symptoms, the timescale and implications of this compensatory process remain an enigma. In order to examine: (i) the nature of the dopaminergic adaptive mechanisms that come into action; (ii) their sequential activation in relation to the severity of degeneration; and (iii) their efficacy with regard to the maintenance of a normal level of basal ganglia activity, we analysed the brains of mice treated daily with 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine (MPTP, 4 mg/kg, i.p.) and killed at 5-day intervals from day 0 (D0) to D20. Our results demonstrate the sequential activation of two compensatory mechanisms: (i) an increase in striatal tyrosine hydroxylase (TH) protein content attested by the persistence of TH immunolabelling up to D15, contrasting with the decrease observed in both the number of nigral TH-immunoreactive neurons (-70.2%) and striatal dopamine content (-38.4%); (ii) a downregulation of DA uptake in surviving terminals at D20 (73.4% of nigral degeneration). At this point, the failure of adaptive mechanisms to maintain striatal dopaminergic homeostasis is also illustrated by an increase in the cytochrome oxidase activity of substantia nigra pars reticulata, a marker of neuronal function. It has been postulated that an increase in dopamine release per pulse could constitute an adaptive mechanism. The data we present from our MPTP mice model infirm this hypothesis. This study explores the link between the degree of nigral degeneration and the sequential activation of dopaminergic compensatory mechanisms in the nigrostriatal pathway and, in so doing, proposes a rethink of the paradigm applied to these mechanisms.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">10971632</PMID><DateCreated><Year>2000</Year><Month>10</Month><Day>19</Day></DateCreated><DateCompleted><Year>2000</Year><Month>10</Month><Day>19</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>12</Volume><Issue>8</Issue><PubDate><Year>2000</Year><Month>Aug</Month></PubDate></JournalIssue><Title>The European journal of neuroscience</Title><ISOAbbreviation>Eur. J. Neurosci.</ISOAbbreviation></Journal><ArticleTitle>Adaptive changes in the nigrostriatal pathway in response to increased 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurodegeneration in the mouse.</ArticleTitle><Pagination><MedlinePgn>2892-900</MedlinePgn></Pagination><Abstract><AbstractText>Although several adaptive mechanisms have been identified that mask the existence of Parkinson's disease and delay the onset and aggravation of motor symptoms, the timescale and implications of this compensatory process remain an enigma. In order to examine: (i) the nature of the dopaminergic adaptive mechanisms that come into action; (ii) their sequential activation in relation to the severity of degeneration; and (iii) their efficacy with regard to the maintenance of a normal level of basal ganglia activity, we analysed the brains of mice treated daily with 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine (MPTP, 4 mg/kg, i.p.) and killed at 5-day intervals from day 0 (D0) to D20. Our results demonstrate the sequential activation of two compensatory mechanisms: (i) an increase in striatal tyrosine hydroxylase (TH) protein content attested by the persistence of TH immunolabelling up to D15, contrasting with the decrease observed in both the number of nigral TH-immunoreactive neurons (-70.2%) and striatal dopamine content (-38.4%); (ii) a downregulation of DA uptake in surviving terminals at D20 (73.4% of nigral degeneration). At this point, the failure of adaptive mechanisms to maintain striatal dopaminergic homeostasis is also illustrated by an increase in the cytochrome oxidase activity of substantia nigra pars reticulata, a marker of neuronal function. It has been postulated that an increase in dopamine release per pulse could constitute an adaptive mechanism. The data we present from our MPTP mice model infirm this hypothesis. This study explores the link between the degree of nigral degeneration and the sequential activation of dopaminergic compensatory mechanisms in the nigrostriatal pathway and, in so doing, proposes a rethink of the paradigm applied to these mechanisms.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bezard</LastName><ForeName>E</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Basal Gang, Laboratoire de Neurophysiologie, CNRS UMR 5543, Université Victor Segalen, 146 rue Léo Saignat, 33076 Bordeaux Cedex, France. erwan.bezard@umr5543.u-bordeaux2.fr</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jaber</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Gonon</LastName><ForeName>F</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Boireau</LastName><ForeName>A</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Bloch</LastName><ForeName>B</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Gross</LastName><ForeName>C E</ForeName><Initials>CE</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>France</Country><MedlineTA>Eur J Neurosci</MedlineTA><NlmUniqueID>8918110</NlmUniqueID><ISSNLinking>0953-816X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D002352">Carrier Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050483">Dopamine Plasma Membrane Transport Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008562">Membrane Glycoproteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D026901">Membrane Transport Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009419">Nerve Tissue Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>10028-17-8</RegistryNumber><NameOfSubstance UI="D014316">Tritium</NameOfSubstance></Chemical><Chemical><RegistryNumber>102-32-9</RegistryNumber><NameOfSubstance UI="D015102">3,4-Dihydroxyphenylacetic Acid</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.16.2</RegistryNumber><NameOfSubstance UI="D014446">Tyrosine 3-Monooxygenase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.9.3.1</RegistryNumber><NameOfSubstance UI="D003576">Electron Transport Complex IV</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical><Chemical><RegistryNumber>X77S6GMS36</RegistryNumber><NameOfSubstance UI="D006719">Homovanillic Acid</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D015102" MajorTopicYN="N">3,4-Dihydroxyphenylacetic Acid</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002352" MajorTopicYN="N">Carrier Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002452" MajorTopicYN="N">Cell Count</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003342" MajorTopicYN="N">Corpus Striatum</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004298" MajorTopicYN="N">Dopamine</DescriptorName><QualifierName UI="Q000493" MajorTopicYN="N">pharmacokinetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050483" MajorTopicYN="N">Dopamine Plasma Membrane Transport Proteins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004558" MajorTopicYN="N">Electric Stimulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003576" MajorTopicYN="N">Electron Transport Complex IV</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004594" MajorTopicYN="N">Electrophysiology</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006719" MajorTopicYN="N">Homovanillic Acid</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020267" MajorTopicYN="N">MPTP Poisoning</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008562" MajorTopicYN="Y">Membrane Glycoproteins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D026901" MajorTopicYN="Y">Membrane Transport Proteins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008815" MajorTopicYN="N">Mice, Inbred Strains</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009410" MajorTopicYN="N">Nerve Degeneration</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009419" MajorTopicYN="Y">Nerve Tissue Proteins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010302" MajorTopicYN="N">Parkinson Disease, Secondary</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013378" MajorTopicYN="N">Substantia Nigra</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013574" MajorTopicYN="N">Synaptosomes</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014316" MajorTopicYN="N">Tritium</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014446" MajorTopicYN="N">Tyrosine 3-Monooxygenase</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2000</Year><Month>9</Month><Day>6</Day><Hour>11</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2000</Year><Month>10</Month><Day>21</Day><Hour>11</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2000</Year><Month>9</Month><Day>6</Day><Hour>11</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">10971632</ArticleId><ArticleId IdType="pii">ejn180</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 001306 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd -nk 001306 | 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:10971632
|texte= Adaptive changes in the nigrostriatal pathway in response to increased 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurodegeneration in the mouse.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/RBID.i -Sk "pubmed:10971632" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd \
| NlmPubMed2Wicri -a ParkinsonFranceV1
| This area was generated with Dilib version V0.6.29. |  |