Striatal molecular signature of subchronic subthalamic nucleus high frequency stimulation in parkinsonian rat.
Identifieur interne : 000747 ( PubMed/Corpus ); précédent : 000746; suivant : 000748Striatal molecular signature of subchronic subthalamic nucleus high frequency stimulation in parkinsonian rat.
Auteurs : Sylviane Lortet ; Emilie Lacombe ; Nicolas Boulanger ; Pascal Rihet ; Catherine Nguyen ; Lydia Kerkerian-Le Goff ; Pascal SalinSource :
- PloS one [ 1932-6203 ] ; 2013.
English descriptors
- KwdEn :
- Animals, Behavior, Animal (drug effects), Cluster Analysis, Corpus Striatum (metabolism), Deep Brain Stimulation, Denervation, Disease Models, Animal, Electric Stimulation, Gene Expression Profiling, Gene Expression Regulation (drug effects), Levodopa (pharmacology), Metabolic Networks and Pathways (genetics), Parkinson Disease (genetics), Parkinson Disease (metabolism), Rats, Subthalamic Nucleus (metabolism).
- MESH :
- chemical , pharmacology : Levodopa.
- drug effects : Behavior, Animal, Gene Expression Regulation.
- genetics : Metabolic Networks and Pathways, Parkinson Disease.
- metabolism : Corpus Striatum, Parkinson Disease, Subthalamic Nucleus.
- Animals, Cluster Analysis, Deep Brain Stimulation, Denervation, Disease Models, Animal, Electric Stimulation, Gene Expression Profiling, Rats.
Abstract
This study addresses the molecular mechanisms underlying the action of subthalamic nucleus high frequency stimulation (STN-HFS) in the treatment of Parkinson's disease and its interaction with levodopa (L-DOPA), focusing on the striatum. Striatal gene expression profile was assessed in rats with nigral dopamine neuron lesion, either treated or not, using agilent microarrays and qPCR verification. The treatments consisted in anti-akinetic STN-HFS (5 days), chronic L-DOPA treatment inducing dyskinesia (LIDs) or the combination of the two treatments that exacerbated LIDs. STN-HFS modulated 71 striatal genes. The main biological processes associated with the differentially expressed gene products include regulation of growth, of apoptosis and of synaptic transmission, and extracellular region is a major cellular component implicated. In particular, several of these genes have been shown to support survival or differentiation of striatal or of dopaminergic neurons. These results indicate that STN HFS may induce widespread anatomo-functional rearrangements in the striatum and create a molecular environment favorable for neuroprotection and neuroplasticity. STN-HFS and L-DOPA treatment share very few common gene regulation features indicating that the molecular substrates underlying their striatal action are mostly different; among the common effects is the down-regulation of Adrb1, which encodes the adrenergic beta-1-receptor, supporting a major role of this receptor in Parkinson's disease. In addition to genes already reported to be associated with LIDs (preprodynorphin, thyrotropin-releasing hormone, metabotropic glutamate receptor 4, cannabinoid receptor 1), the comparison between DOPA and DOPA/HFS identifies immunity-related genes as potential players in L-DOPA side effects.
DOI: 10.1371/journal.pone.0060447
PubMed: 23593219
Links to Exploration step
pubmed:23593219Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Striatal molecular signature of subchronic subthalamic nucleus high frequency stimulation in parkinsonian rat.</title><author><name sortKey="Lortet, Sylviane" sort="Lortet, Sylviane" uniqKey="Lortet S" first="Sylviane" last="Lortet">Sylviane Lortet</name><affiliation><nlm:affiliation>Aix-Marseille Université, CNRS, IBDM UMR 7288, Marseille, France. sylviane.lortet@univ-amu.fr</nlm:affiliation></affiliation></author><author><name sortKey="Lacombe, Emilie" sort="Lacombe, Emilie" uniqKey="Lacombe E" first="Emilie" last="Lacombe">Emilie Lacombe</name></author><author><name sortKey="Boulanger, Nicolas" sort="Boulanger, Nicolas" uniqKey="Boulanger N" first="Nicolas" last="Boulanger">Nicolas Boulanger</name></author><author><name sortKey="Rihet, Pascal" sort="Rihet, Pascal" uniqKey="Rihet P" first="Pascal" last="Rihet">Pascal Rihet</name></author><author><name sortKey="Nguyen, Catherine" sort="Nguyen, Catherine" uniqKey="Nguyen C" first="Catherine" last="Nguyen">Catherine Nguyen</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></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2013">2013</date><idno type="RBID">pubmed:23593219</idno><idno type="pmid">23593219</idno><idno type="doi">10.1371/journal.pone.0060447</idno><idno type="wicri:Area/PubMed/Corpus">000747</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000747</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Striatal molecular signature of subchronic subthalamic nucleus high frequency stimulation in parkinsonian rat.</title><author><name sortKey="Lortet, Sylviane" sort="Lortet, Sylviane" uniqKey="Lortet S" first="Sylviane" last="Lortet">Sylviane Lortet</name><affiliation><nlm:affiliation>Aix-Marseille Université, CNRS, IBDM UMR 7288, Marseille, France. sylviane.lortet@univ-amu.fr</nlm:affiliation></affiliation></author><author><name sortKey="Lacombe, Emilie" sort="Lacombe, Emilie" uniqKey="Lacombe E" first="Emilie" last="Lacombe">Emilie Lacombe</name></author><author><name sortKey="Boulanger, Nicolas" sort="Boulanger, Nicolas" uniqKey="Boulanger N" first="Nicolas" last="Boulanger">Nicolas Boulanger</name></author><author><name sortKey="Rihet, Pascal" sort="Rihet, Pascal" uniqKey="Rihet P" first="Pascal" last="Rihet">Pascal Rihet</name></author><author><name sortKey="Nguyen, Catherine" sort="Nguyen, Catherine" uniqKey="Nguyen C" first="Catherine" last="Nguyen">Catherine Nguyen</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">PloS one</title><idno type="eISSN">1932-6203</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Behavior, Animal (drug effects)</term><term>Cluster Analysis</term><term>Corpus Striatum (metabolism)</term><term>Deep Brain Stimulation</term><term>Denervation</term><term>Disease Models, Animal</term><term>Electric Stimulation</term><term>Gene Expression Profiling</term><term>Gene Expression Regulation (drug effects)</term><term>Levodopa (pharmacology)</term><term>Metabolic Networks and Pathways (genetics)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (metabolism)</term><term>Rats</term><term>Subthalamic Nucleus (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Behavior, Animal</term><term>Gene Expression Regulation</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Metabolic Networks and Pathways</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Corpus Striatum</term><term>Parkinson Disease</term><term>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cluster Analysis</term><term>Deep Brain Stimulation</term><term>Denervation</term><term>Disease Models, Animal</term><term>Electric Stimulation</term><term>Gene Expression Profiling</term><term>Rats</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">This study addresses the molecular mechanisms underlying the action of subthalamic nucleus high frequency stimulation (STN-HFS) in the treatment of Parkinson's disease and its interaction with levodopa (L-DOPA), focusing on the striatum. Striatal gene expression profile was assessed in rats with nigral dopamine neuron lesion, either treated or not, using agilent microarrays and qPCR verification. The treatments consisted in anti-akinetic STN-HFS (5 days), chronic L-DOPA treatment inducing dyskinesia (LIDs) or the combination of the two treatments that exacerbated LIDs. STN-HFS modulated 71 striatal genes. The main biological processes associated with the differentially expressed gene products include regulation of growth, of apoptosis and of synaptic transmission, and extracellular region is a major cellular component implicated. In particular, several of these genes have been shown to support survival or differentiation of striatal or of dopaminergic neurons. These results indicate that STN HFS may induce widespread anatomo-functional rearrangements in the striatum and create a molecular environment favorable for neuroprotection and neuroplasticity. STN-HFS and L-DOPA treatment share very few common gene regulation features indicating that the molecular substrates underlying their striatal action are mostly different; among the common effects is the down-regulation of Adrb1, which encodes the adrenergic beta-1-receptor, supporting a major role of this receptor in Parkinson's disease. In addition to genes already reported to be associated with LIDs (preprodynorphin, thyrotropin-releasing hormone, metabotropic glutamate receptor 4, cannabinoid receptor 1), the comparison between DOPA and DOPA/HFS identifies immunity-related genes as potential players in L-DOPA side effects.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23593219</PMID><DateCreated><Year>2013</Year><Month>04</Month><Day>17</Day></DateCreated><DateCompleted><Year>2013</Year><Month>11</Month><Day>04</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>05</Day></DateRevised><Article PubModel="Electronic-Print"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>8</Volume><Issue>4</Issue><PubDate><Year>2013</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS ONE</ISOAbbreviation></Journal><ArticleTitle>Striatal molecular signature of subchronic subthalamic nucleus high frequency stimulation in parkinsonian rat.</ArticleTitle><Pagination><MedlinePgn>e60447</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0060447</ELocationID><Abstract><AbstractText>This study addresses the molecular mechanisms underlying the action of subthalamic nucleus high frequency stimulation (STN-HFS) in the treatment of Parkinson's disease and its interaction with levodopa (L-DOPA), focusing on the striatum. Striatal gene expression profile was assessed in rats with nigral dopamine neuron lesion, either treated or not, using agilent microarrays and qPCR verification. The treatments consisted in anti-akinetic STN-HFS (5 days), chronic L-DOPA treatment inducing dyskinesia (LIDs) or the combination of the two treatments that exacerbated LIDs. STN-HFS modulated 71 striatal genes. The main biological processes associated with the differentially expressed gene products include regulation of growth, of apoptosis and of synaptic transmission, and extracellular region is a major cellular component implicated. In particular, several of these genes have been shown to support survival or differentiation of striatal or of dopaminergic neurons. These results indicate that STN HFS may induce widespread anatomo-functional rearrangements in the striatum and create a molecular environment favorable for neuroprotection and neuroplasticity. STN-HFS and L-DOPA treatment share very few common gene regulation features indicating that the molecular substrates underlying their striatal action are mostly different; among the common effects is the down-regulation of Adrb1, which encodes the adrenergic beta-1-receptor, supporting a major role of this receptor in Parkinson's disease. In addition to genes already reported to be associated with LIDs (preprodynorphin, thyrotropin-releasing hormone, metabotropic glutamate receptor 4, cannabinoid receptor 1), the comparison between DOPA and DOPA/HFS identifies immunity-related genes as potential players in L-DOPA side effects.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lortet</LastName><ForeName>Sylviane</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Aix-Marseille Université, CNRS, IBDM UMR 7288, Marseille, France. sylviane.lortet@univ-amu.fr</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lacombe</LastName><ForeName>Emilie</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Boulanger</LastName><ForeName>Nicolas</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Rihet</LastName><ForeName>Pascal</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Nguyen</LastName><ForeName>Catherine</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Kerkerian-Le Goff</LastName><ForeName>Lydia</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Salin</LastName><ForeName>Pascal</ForeName><Initials>P</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><ArticleDate DateType="Electronic"><Year>2013</Year><Month>04</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance 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MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC3617149</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2012</Year><Month>11</Month><Day>06</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2013</Year><Month>02</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2013</Year><Month>4</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2013</Year><Month>4</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2013</Year><Month>11</Month><Day>5</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">23593219</ArticleId><ArticleId IdType="doi">10.1371/journal.pone.0060447</ArticleId><ArticleId IdType="pii">PONE-D-12-36103</ArticleId><ArticleId 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