Deep brain stimulation of the subthalamic nucleus preferentially alters the translational profile of striatopallidal neurons in an animal model of Parkinson's disease.
Identifieur interne : 000480 ( PubMed/Corpus ); précédent : 000479; suivant : 000481Deep brain stimulation of the subthalamic nucleus preferentially alters the translational profile of striatopallidal neurons in an animal model of Parkinson's disease.
Auteurs : Naomi P. Visanji ; Iman Kamali Sarvestani ; Meaghan C. Creed ; Zahra Shams Shoaei ; José N. Nobrega ; Clement Hamani ; Lili-Naz HazratiSource :
- Frontiers in cellular neuroscience ; 2015.
Abstract
Deep brain stimulation targeting the subthalamic nucleus (STN-DBS) is an effective surgical treatment for the motor symptoms of Parkinson's disease (PD), the precise neuronal mechanisms of which both at molecular and network levels remain a topic of debate. Here we employ two transgenic mouse lines, combining translating ribosomal affinity purification (TRAP) with bacterial artificial chromosome expression (Bac), to selectively identify changes in translational gene expression in either Drd1a-expressing striatonigral or Drd2-expressing striatopallidal medium spiny neurons (MSNs) of the striatum following STN-DBS. 6-hydroxydopamine lesioned mice received either 5 days stimulation via a DBS electrode implanted in the ipsilateral STN or 5 days sham treatment (no stimulation). Striatal polyribosomal RNA was selectively purified from either Drd2 or Drd1a MSNs using the TRAP method and gene expression profiling performed. We identified eight significantly altered genes in Drd2 MSNs (Vps33b, Ppp1r3c, Mapk4, Sorcs2, Neto1, Abca1, Penk1, and Gapdh) and two overlapping genes in Drd1a MSNs (Penk1 and Ppp1r3c) implicated in the molecular mechanisms of STN-DBS. A detailed functional analysis, using a further 728 probes implicated in STN-DBS, suggested an increased ability to receive excitation (mediated by increased dendritic spines, increased calcium influx and enhanced excitatory post synaptic potentials) accompanied by processes that would hamper the initiation of action potentials, transport of neurotransmitters from soma to axon terminals and vesicular release in Drd2-expressing MSNs. Finally, changes in expression of several genes involved in apoptosis as well as cholesterol and fatty acid metabolism were also identified. This increased understanding of the molecular mechanisms induced by STN-DBS may reveal novel targets for future non-surgical therapies for PD.
DOI: 10.3389/fncel.2015.00221
PubMed: 26106299
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Safra Program in Parkinson's disease, Toronto Western Hospital Toronto, ON, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Kamali Sarvestani, Iman" sort="Kamali Sarvestani, Iman" uniqKey="Kamali Sarvestani I" first="Iman" last="Kamali Sarvestani">Iman Kamali Sarvestani</name><affiliation><nlm:affiliation>Faculty of Medicine, Tanz Centre for Research in Neurodegenerative Diseases, University of Toronto Toronto, ON, Canada ; Department of Neuroscience, Stockholm Brain Institute, Karolinska Institute Stockholm, Sweden.</nlm:affiliation></affiliation></author><author><name sortKey="Creed, Meaghan C" sort="Creed, Meaghan C" uniqKey="Creed M" first="Meaghan C" last="Creed">Meaghan C. 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Nobrega</name><affiliation><nlm:affiliation>Behavioural Neurobiology Laboratory, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health Toronto, ON, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Hamani, Clement" sort="Hamani, Clement" uniqKey="Hamani C" first="Clement" last="Hamani">Clement Hamani</name><affiliation><nlm:affiliation>Behavioural Neurobiology Laboratory, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health Toronto, ON, Canada ; Division of Neurosurgery, Toronto Western Hospital, University of Toronto Toronto, ON, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Hazrati, Lili Naz" sort="Hazrati, Lili Naz" uniqKey="Hazrati L" first="Lili-Naz" last="Hazrati">Lili-Naz Hazrati</name><affiliation><nlm:affiliation>Faculty of Medicine, Tanz Centre for Research in Neurodegenerative Diseases, University of Toronto Toronto, ON, Canada.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2015">2015</date><idno type="RBID">pubmed:26106299</idno><idno type="pmid">26106299</idno><idno type="doi">10.3389/fncel.2015.00221</idno><idno type="wicri:Area/PubMed/Corpus">000480</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000480</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Deep brain stimulation of the subthalamic nucleus preferentially alters the translational profile of striatopallidal neurons in an animal model of Parkinson's disease.</title><author><name sortKey="Visanji, Naomi P" sort="Visanji, Naomi P" uniqKey="Visanji N" first="Naomi P" last="Visanji">Naomi P. Visanji</name><affiliation><nlm:affiliation>Morton and Gloria Shulman Movement Disorders Centre and the Edmund J. Safra Program in Parkinson's disease, Toronto Western Hospital Toronto, ON, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Kamali Sarvestani, Iman" sort="Kamali Sarvestani, Iman" uniqKey="Kamali Sarvestani I" first="Iman" last="Kamali Sarvestani">Iman Kamali Sarvestani</name><affiliation><nlm:affiliation>Faculty of Medicine, Tanz Centre for Research in Neurodegenerative Diseases, University of Toronto Toronto, ON, Canada ; Department of Neuroscience, Stockholm Brain Institute, Karolinska Institute Stockholm, Sweden.</nlm:affiliation></affiliation></author><author><name sortKey="Creed, Meaghan C" sort="Creed, Meaghan C" uniqKey="Creed M" first="Meaghan C" last="Creed">Meaghan C. Creed</name><affiliation><nlm:affiliation>Behavioural Neurobiology Laboratory, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health Toronto, ON, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Shams Shoaei, Zahra" sort="Shams Shoaei, Zahra" uniqKey="Shams Shoaei Z" first="Zahra" last="Shams Shoaei">Zahra Shams Shoaei</name><affiliation><nlm:affiliation>Faculty of Medicine, Tanz Centre for Research in Neurodegenerative Diseases, University of Toronto Toronto, ON, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Nobrega, Jose N" sort="Nobrega, Jose N" uniqKey="Nobrega J" first="José N" last="Nobrega">José N. Nobrega</name><affiliation><nlm:affiliation>Behavioural Neurobiology Laboratory, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health Toronto, ON, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Hamani, Clement" sort="Hamani, Clement" uniqKey="Hamani C" first="Clement" last="Hamani">Clement Hamani</name><affiliation><nlm:affiliation>Behavioural Neurobiology Laboratory, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health Toronto, ON, Canada ; Division of Neurosurgery, Toronto Western Hospital, University of Toronto Toronto, ON, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Hazrati, Lili Naz" sort="Hazrati, Lili Naz" uniqKey="Hazrati L" first="Lili-Naz" last="Hazrati">Lili-Naz Hazrati</name><affiliation><nlm:affiliation>Faculty of Medicine, Tanz Centre for Research in Neurodegenerative Diseases, University of Toronto Toronto, ON, Canada.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Frontiers in cellular neuroscience</title><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Deep brain stimulation targeting the subthalamic nucleus (STN-DBS) is an effective surgical treatment for the motor symptoms of Parkinson's disease (PD), the precise neuronal mechanisms of which both at molecular and network levels remain a topic of debate. Here we employ two transgenic mouse lines, combining translating ribosomal affinity purification (TRAP) with bacterial artificial chromosome expression (Bac), to selectively identify changes in translational gene expression in either Drd1a-expressing striatonigral or Drd2-expressing striatopallidal medium spiny neurons (MSNs) of the striatum following STN-DBS. 6-hydroxydopamine lesioned mice received either 5 days stimulation via a DBS electrode implanted in the ipsilateral STN or 5 days sham treatment (no stimulation). Striatal polyribosomal RNA was selectively purified from either Drd2 or Drd1a MSNs using the TRAP method and gene expression profiling performed. We identified eight significantly altered genes in Drd2 MSNs (Vps33b, Ppp1r3c, Mapk4, Sorcs2, Neto1, Abca1, Penk1, and Gapdh) and two overlapping genes in Drd1a MSNs (Penk1 and Ppp1r3c) implicated in the molecular mechanisms of STN-DBS. A detailed functional analysis, using a further 728 probes implicated in STN-DBS, suggested an increased ability to receive excitation (mediated by increased dendritic spines, increased calcium influx and enhanced excitatory post synaptic potentials) accompanied by processes that would hamper the initiation of action potentials, transport of neurotransmitters from soma to axon terminals and vesicular release in Drd2-expressing MSNs. Finally, changes in expression of several genes involved in apoptosis as well as cholesterol and fatty acid metabolism were also identified. This increased understanding of the molecular mechanisms induced by STN-DBS may reveal novel targets for future non-surgical therapies for PD.</div></front></TEI><pubmed><MedlineCitation Status="PubMed-not-MEDLINE" Owner="NLM"><PMID Version="1">26106299</PMID><DateCreated><Year>2015</Year><Month>06</Month><Day>24</Day></DateCreated><DateCompleted><Year>2015</Year><Month>06</Month><Day>24</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><JournalIssue CitedMedium="Print"><Volume>9</Volume><PubDate><Year>2015</Year></PubDate></JournalIssue><Title>Frontiers in cellular neuroscience</Title><ISOAbbreviation>Front Cell Neurosci</ISOAbbreviation></Journal><ArticleTitle>Deep brain stimulation of the subthalamic nucleus preferentially alters the translational profile of striatopallidal neurons in an animal model of Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>221</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3389/fncel.2015.00221</ELocationID><Abstract><AbstractText>Deep brain stimulation targeting the subthalamic nucleus (STN-DBS) is an effective surgical treatment for the motor symptoms of Parkinson's disease (PD), the precise neuronal mechanisms of which both at molecular and network levels remain a topic of debate. Here we employ two transgenic mouse lines, combining translating ribosomal affinity purification (TRAP) with bacterial artificial chromosome expression (Bac), to selectively identify changes in translational gene expression in either Drd1a-expressing striatonigral or Drd2-expressing striatopallidal medium spiny neurons (MSNs) of the striatum following STN-DBS. 6-hydroxydopamine lesioned mice received either 5 days stimulation via a DBS electrode implanted in the ipsilateral STN or 5 days sham treatment (no stimulation). Striatal polyribosomal RNA was selectively purified from either Drd2 or Drd1a MSNs using the TRAP method and gene expression profiling performed. We identified eight significantly altered genes in Drd2 MSNs (Vps33b, Ppp1r3c, Mapk4, Sorcs2, Neto1, Abca1, Penk1, and Gapdh) and two overlapping genes in Drd1a MSNs (Penk1 and Ppp1r3c) implicated in the molecular mechanisms of STN-DBS. A detailed functional analysis, using a further 728 probes implicated in STN-DBS, suggested an increased ability to receive excitation (mediated by increased dendritic spines, increased calcium influx and enhanced excitatory post synaptic potentials) accompanied by processes that would hamper the initiation of action potentials, transport of neurotransmitters from soma to axon terminals and vesicular release in Drd2-expressing MSNs. Finally, changes in expression of several genes involved in apoptosis as well as cholesterol and fatty acid metabolism were also identified. This increased understanding of the molecular mechanisms induced by STN-DBS may reveal novel targets for future non-surgical therapies for PD.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Visanji</LastName><ForeName>Naomi P</ForeName><Initials>NP</Initials><AffiliationInfo><Affiliation>Morton and Gloria Shulman Movement Disorders Centre and the Edmund J. Safra Program in Parkinson's disease, Toronto Western Hospital Toronto, ON, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kamali Sarvestani</LastName><ForeName>Iman</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Faculty of Medicine, Tanz Centre for Research in Neurodegenerative Diseases, University of Toronto Toronto, ON, Canada ; Department of Neuroscience, Stockholm Brain Institute, Karolinska Institute Stockholm, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Creed</LastName><ForeName>Meaghan C</ForeName><Initials>MC</Initials><AffiliationInfo><Affiliation>Behavioural Neurobiology Laboratory, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health Toronto, ON, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shams Shoaei</LastName><ForeName>Zahra</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Faculty of Medicine, Tanz Centre for Research in Neurodegenerative Diseases, University of Toronto Toronto, ON, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nobrega</LastName><ForeName>José N</ForeName><Initials>JN</Initials><AffiliationInfo><Affiliation>Behavioural Neurobiology Laboratory, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health Toronto, ON, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hamani</LastName><ForeName>Clement</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Behavioural Neurobiology Laboratory, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health Toronto, ON, Canada ; Division of Neurosurgery, Toronto Western Hospital, University of Toronto Toronto, ON, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hazrati</LastName><ForeName>Lili-Naz</ForeName><Initials>LN</Initials><AffiliationInfo><Affiliation>Faculty of Medicine, 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MajorTopicYN="N">Parkinson's disease</Keyword><Keyword MajorTopicYN="N">deep brain stimulation</Keyword><Keyword MajorTopicYN="N">striatal medium spiny neurons</Keyword><Keyword MajorTopicYN="N">subthalamic nucleus</Keyword><Keyword MajorTopicYN="N">translational profile</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>03</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>05</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>6</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>6</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>6</Month><Day>25</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26106299</ArticleId><ArticleId IdType="doi">10.3389/fncel.2015.00221</ArticleId><ArticleId IdType="pmc">PMC4460554</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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