Unilateral lesion of the nigrostriatal pathway induces an increase of neuronal activity of the pedunculopontine nucleus, which is reversed by the lesion of the subthalamic nucleus in the rat.
Identifieur interne : 001222 ( PubMed/Corpus ); précédent : 001221; suivant : 001223Unilateral lesion of the nigrostriatal pathway induces an increase of neuronal activity of the pedunculopontine nucleus, which is reversed by the lesion of the subthalamic nucleus in the rat.
Auteurs : S. Breit ; R. Bouali-Benazzouz ; A L Benabid ; A. BenazzouzSource :
- The European journal of neuroscience [ 0953-816X ] ; 2001.
English descriptors
- KwdEn :
- Action Potentials (physiology), Animals, Cholinergic Fibers (metabolism), Functional Laterality (physiology), Immunohistochemistry, Male, Neural Pathways (injuries), Neural Pathways (pathology), Neural Pathways (physiopathology), Neurons (metabolism), Parkinson Disease (pathology), Parkinson Disease (physiopathology), Rats, Rats, Wistar, Substantia Nigra (injuries), Substantia Nigra (pathology), Substantia Nigra (physiopathology), Subthalamic Nucleus (injuries), Subthalamic Nucleus (pathology), Subthalamic Nucleus (physiopathology), Tegmentum Mesencephali (physiopathology).
- MESH :
- injuries : Neural Pathways, Substantia Nigra, Subthalamic Nucleus.
- metabolism : Cholinergic Fibers, Neurons.
- pathology : Neural Pathways, Parkinson Disease, Substantia Nigra, Subthalamic Nucleus.
- physiology : Action Potentials, Functional Laterality.
- physiopathology : Neural Pathways, Parkinson Disease, Substantia Nigra, Subthalamic Nucleus, Tegmentum Mesencephali.
- Animals, Immunohistochemistry, Male, Rats, Rats, Wistar.
Abstract
The role of the pedunculopontine nucleus (PPN) in the pathophysiology of Parkinson's disease is still unclear. Using microrecordings, we investigated the changes occurring in PPN neurons after lesions of the substantia nigra compacta (SNc) and the role of the subthalamic nucleus (STN) in these changes. In normal rats the firing rate of PPN neurons was 10.6 +/- 1.4 spikes/s, the majority of neurons (91%) having a regular firing pattern, 6% irregular and 3% in bursts. In rats with 6-hydroxydopamine lesions of the SNc, the firing rate increased significantly to 18.3 +/- 3.0 spikes/s compared with normal rats. In addition, the firing pattern changed significantly: 70% of the neurons discharged regularly, 27% irregularly and 3% in bursts. In rats with ibotenic acid lesions of the STN, the firing rate decreased significantly to 7.2 +/- 0.9 spikes/s and the firing pattern changed significantly: 50% of the neurons discharged regularly, 43% irregularly and 7% in bursts. The rats with combined SNc and STN lesions showed no change in the firing rate (8.5 +/- 1.0 spikes/s) compared to normal rats. The firing pattern changed significantly: 69% of the cells discharged regularly, 26% irregularly and 5% in bursts. These findings demonstrate that PPN neurons are overactive and more irregular in the 6-hydroxydopamine-lesioned rats, suggesting the implication of this nucleus in the pathophysiology of parkinsonism. Moreover, the fact that STN lesions induced a reduction in the firing rate of the PPN in normal rats and a normalization of the firing rate in rats with 6-hydroxydopamine lesions suggests that this nucleus is under major control of the STN.
PubMed: 11860479
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Unilateral lesion of the nigrostriatal pathway induces an increase of neuronal activity of the pedunculopontine nucleus, which is reversed by the lesion of the subthalamic nucleus in the rat.</title><author><name sortKey="Breit, S" sort="Breit, S" uniqKey="Breit S" first="S" last="Breit">S. Breit</name><affiliation><nlm:affiliation>INSERM U318, Laboratoire de Neuroscience Preclinique, CHU-Pavillon B, BP 217, 38043 Grenoble cedex 09, France.</nlm:affiliation></affiliation></author><author><name sortKey="Bouali Benazzouz, R" sort="Bouali Benazzouz, R" uniqKey="Bouali Benazzouz R" first="R" last="Bouali-Benazzouz">R. Bouali-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><author><name sortKey="Benazzouz, A" sort="Benazzouz, A" uniqKey="Benazzouz A" first="A" last="Benazzouz">A. Benazzouz</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2001">2001</date><idno type="RBID">pubmed:11860479</idno><idno type="pmid">11860479</idno><idno type="wicri:Area/PubMed/Corpus">001222</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001222</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Unilateral lesion of the nigrostriatal pathway induces an increase of neuronal activity of the pedunculopontine nucleus, which is reversed by the lesion of the subthalamic nucleus in the rat.</title><author><name sortKey="Breit, S" sort="Breit, S" uniqKey="Breit S" first="S" last="Breit">S. Breit</name><affiliation><nlm:affiliation>INSERM U318, Laboratoire de Neuroscience Preclinique, CHU-Pavillon B, BP 217, 38043 Grenoble cedex 09, France.</nlm:affiliation></affiliation></author><author><name sortKey="Bouali Benazzouz, R" sort="Bouali Benazzouz, R" uniqKey="Bouali Benazzouz R" first="R" last="Bouali-Benazzouz">R. Bouali-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><author><name sortKey="Benazzouz, A" sort="Benazzouz, A" uniqKey="Benazzouz A" first="A" last="Benazzouz">A. Benazzouz</name></author></analytic><series><title level="j">The European journal of neuroscience</title><idno type="ISSN">0953-816X</idno><imprint><date when="2001" type="published">2001</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Action Potentials (physiology)</term><term>Animals</term><term>Cholinergic Fibers (metabolism)</term><term>Functional Laterality (physiology)</term><term>Immunohistochemistry</term><term>Male</term><term>Neural Pathways (injuries)</term><term>Neural Pathways (pathology)</term><term>Neural Pathways (physiopathology)</term><term>Neurons (metabolism)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (physiopathology)</term><term>Rats</term><term>Rats, Wistar</term><term>Substantia Nigra (injuries)</term><term>Substantia Nigra (pathology)</term><term>Substantia Nigra (physiopathology)</term><term>Subthalamic Nucleus (injuries)</term><term>Subthalamic Nucleus (pathology)</term><term>Subthalamic Nucleus (physiopathology)</term><term>Tegmentum Mesencephali (physiopathology)</term></keywords><keywords scheme="MESH" qualifier="injuries" xml:lang="en"><term>Neural Pathways</term><term>Substantia Nigra</term><term>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cholinergic Fibers</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Neural Pathways</term><term>Parkinson Disease</term><term>Substantia Nigra</term><term>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Action Potentials</term><term>Functional Laterality</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Neural Pathways</term><term>Parkinson Disease</term><term>Substantia Nigra</term><term>Subthalamic Nucleus</term><term>Tegmentum Mesencephali</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Immunohistochemistry</term><term>Male</term><term>Rats</term><term>Rats, Wistar</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The role of the pedunculopontine nucleus (PPN) in the pathophysiology of Parkinson's disease is still unclear. Using microrecordings, we investigated the changes occurring in PPN neurons after lesions of the substantia nigra compacta (SNc) and the role of the subthalamic nucleus (STN) in these changes. In normal rats the firing rate of PPN neurons was 10.6 +/- 1.4 spikes/s, the majority of neurons (91%) having a regular firing pattern, 6% irregular and 3% in bursts. In rats with 6-hydroxydopamine lesions of the SNc, the firing rate increased significantly to 18.3 +/- 3.0 spikes/s compared with normal rats. In addition, the firing pattern changed significantly: 70% of the neurons discharged regularly, 27% irregularly and 3% in bursts. In rats with ibotenic acid lesions of the STN, the firing rate decreased significantly to 7.2 +/- 0.9 spikes/s and the firing pattern changed significantly: 50% of the neurons discharged regularly, 43% irregularly and 7% in bursts. The rats with combined SNc and STN lesions showed no change in the firing rate (8.5 +/- 1.0 spikes/s) compared to normal rats. The firing pattern changed significantly: 69% of the cells discharged regularly, 26% irregularly and 5% in bursts. These findings demonstrate that PPN neurons are overactive and more irregular in the 6-hydroxydopamine-lesioned rats, suggesting the implication of this nucleus in the pathophysiology of parkinsonism. Moreover, the fact that STN lesions induced a reduction in the firing rate of the PPN in normal rats and a normalization of the firing rate in rats with 6-hydroxydopamine lesions suggests that this nucleus is under major control of the STN.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">11860479</PMID><DateCreated><Year>2002</Year><Month>02</Month><Day>25</Day></DateCreated><DateCompleted><Year>2002</Year><Month>04</Month><Day>05</Day></DateCompleted><DateRevised><Year>2006</Year><Month>11</Month><Day>15</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0953-816X</ISSN><JournalIssue CitedMedium="Print"><Volume>14</Volume><Issue>11</Issue><PubDate><Year>2001</Year><Month>Dec</Month></PubDate></JournalIssue><Title>The European journal of neuroscience</Title><ISOAbbreviation>Eur. J. Neurosci.</ISOAbbreviation></Journal><ArticleTitle>Unilateral lesion of the nigrostriatal pathway induces an increase of neuronal activity of the pedunculopontine nucleus, which is reversed by the lesion of the subthalamic nucleus in the rat.</ArticleTitle><Pagination><MedlinePgn>1833-42</MedlinePgn></Pagination><Abstract><AbstractText>The role of the pedunculopontine nucleus (PPN) in the pathophysiology of Parkinson's disease is still unclear. Using microrecordings, we investigated the changes occurring in PPN neurons after lesions of the substantia nigra compacta (SNc) and the role of the subthalamic nucleus (STN) in these changes. In normal rats the firing rate of PPN neurons was 10.6 +/- 1.4 spikes/s, the majority of neurons (91%) having a regular firing pattern, 6% irregular and 3% in bursts. In rats with 6-hydroxydopamine lesions of the SNc, the firing rate increased significantly to 18.3 +/- 3.0 spikes/s compared with normal rats. In addition, the firing pattern changed significantly: 70% of the neurons discharged regularly, 27% irregularly and 3% in bursts. In rats with ibotenic acid lesions of the STN, the firing rate decreased significantly to 7.2 +/- 0.9 spikes/s and the firing pattern changed significantly: 50% of the neurons discharged regularly, 43% irregularly and 7% in bursts. The rats with combined SNc and STN lesions showed no change in the firing rate (8.5 +/- 1.0 spikes/s) compared to normal rats. The firing pattern changed significantly: 69% of the cells discharged regularly, 26% irregularly and 5% in bursts. These findings demonstrate that PPN neurons are overactive and more irregular in the 6-hydroxydopamine-lesioned rats, suggesting the implication of this nucleus in the pathophysiology of parkinsonism. Moreover, the fact that STN lesions induced a reduction in the firing rate of the PPN in normal rats and a normalization of the firing rate in rats with 6-hydroxydopamine lesions suggests that this nucleus is under major control of the STN.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Breit</LastName><ForeName>S</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>INSERM U318, Laboratoire de Neuroscience Preclinique, CHU-Pavillon B, BP 217, 38043 Grenoble cedex 09, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bouali-Benazzouz</LastName><ForeName>R</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Benabid</LastName><ForeName>A L</ForeName><Initials>AL</Initials></Author><Author ValidYN="Y"><LastName>Benazzouz</LastName><ForeName>A</ForeName><Initials>A</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><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000200" MajorTopicYN="N">Action Potentials</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002799" MajorTopicYN="N">Cholinergic Fibers</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007839" MajorTopicYN="N">Functional Laterality</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007150" MajorTopicYN="N">Immunohistochemistry</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009434" MajorTopicYN="N">Neural Pathways</DescriptorName><QualifierName UI="Q000293" MajorTopicYN="N">injuries</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017208" MajorTopicYN="N">Rats, Wistar</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013378" MajorTopicYN="N">Substantia Nigra</DescriptorName><QualifierName UI="Q000293" MajorTopicYN="N">injuries</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020531" MajorTopicYN="N">Subthalamic Nucleus</DescriptorName><QualifierName UI="Q000293" MajorTopicYN="N">injuries</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013681" MajorTopicYN="N">Tegmentum Mesencephali</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2002</Year><Month>2</Month><Day>28</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2002</Year><Month>4</Month><Day>6</Day><Hour>10</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2002</Year><Month>2</Month><Day>28</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">11860479</ArticleId><ArticleId IdType="pii">1800</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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