Subthalamic Nucleus Neuronal Firing Rate Increases with Parkinson’s Disease Progression
Identifieur interne : 000120 ( Pmc/Checkpoint ); précédent : 000119; suivant : 000121Subthalamic Nucleus Neuronal Firing Rate Increases with Parkinson’s Disease Progression
Auteurs : Michael Remple ; Courtney Bradenham ; C Kao ; P Charles ; Joseph Neimat ; Peter KonradSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2011.
Abstract
Parkinson’s disease (PD) is a neurodegenerative disorder characterized by progressive loss of dopaminergic cells in the central nervous system, in particular the substantia nigra, resulting in an unrelenting loss of motor and non-motor function. Animal models of PD reveal hyperactive neurons in the subthalamic nucleus (STN) that have increased firing rates and bursting activity compared to controls. Although STN activity has been characterized in advanced stage PD patients, it has not been described in early stage PD patients. Here we present the results of STN neuronal recordings from early stage PD patients (Hoehn and Yahr stage II) enrolled in an ongoing clinical trial compared to recordings from age and sex matched advanced PD patients. STN neurons had a significantly lower firing rate in early versus advanced PD (28.7Hz vs. 36.3Hz; p<0.01). The overall activity of the STN was also significantly lower in early versus late PD, as measured by background neuronal noise (12.4mV vs. 14.0mV; p <0.05). No significant difference was identified between groups in the bursting or variability of neuronal firing in the STN, as measured by a burst index or the interspike interval coefficient of variability. The results suggest that neuronal firing in STN increases with PD progression.
Url:
DOI: 10.1002/mds.23708
PubMed: 21542021
PubMed Central: 3151310
Affiliations:
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Neurosurgery, Vanderbilt University Medical Center, Nashville TN</nlm:aff><wicri:noCountry code="subfield">Nashville TN</wicri:noCountry></affiliation></author><author><name sortKey="Charles, P David" sort="Charles, P David" uniqKey="Charles P" first="P" last="Charles">P Charles</name><affiliation><nlm:aff id="A2"> Dept of Neurology, Vanderbilt University Medical Center, Nashville TN</nlm:aff><wicri:noCountry code="subfield">Nashville TN</wicri:noCountry></affiliation></author><author><name sortKey="Neimat, Joseph S" sort="Neimat, Joseph S" uniqKey="Neimat J" first="Joseph" last="Neimat">Joseph Neimat</name><affiliation><nlm:aff id="A1"> Dept of Neurosurgery, Vanderbilt University Medical Center, Nashville TN</nlm:aff><wicri:noCountry code="subfield">Nashville TN</wicri:noCountry></affiliation></author><author><name sortKey="Konrad, Peter E" sort="Konrad, Peter E" uniqKey="Konrad P" first="Peter" last="Konrad">Peter Konrad</name><affiliation><nlm:aff id="A1"> Dept of Neurosurgery, 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University Medical Center, Nashville TN</nlm:aff><wicri:noCountry code="subfield">Nashville TN</wicri:noCountry></affiliation></author><author><name sortKey="Bradenham, Courtney H" sort="Bradenham, Courtney H" uniqKey="Bradenham C" first="Courtney" last="Bradenham">Courtney Bradenham</name><affiliation><nlm:aff id="A2"> Dept of Neurology, Vanderbilt University Medical Center, Nashville TN</nlm:aff><wicri:noCountry code="subfield">Nashville TN</wicri:noCountry></affiliation></author><author><name sortKey="Kao, C Chris" sort="Kao, C Chris" uniqKey="Kao C" first="C" last="Kao">C Kao</name><affiliation><nlm:aff id="A1"> Dept of Neurosurgery, Vanderbilt University Medical Center, Nashville TN</nlm:aff><wicri:noCountry code="subfield">Nashville TN</wicri:noCountry></affiliation></author><author><name sortKey="Charles, P David" sort="Charles, P David" uniqKey="Charles P" first="P" last="Charles">P Charles</name><affiliation><nlm:aff id="A2"> Dept of Neurology, Vanderbilt University Medical Center, Nashville TN</nlm:aff><wicri:noCountry code="subfield">Nashville TN</wicri:noCountry></affiliation></author><author><name sortKey="Neimat, Joseph S" sort="Neimat, Joseph S" uniqKey="Neimat J" first="Joseph" last="Neimat">Joseph Neimat</name><affiliation><nlm:aff id="A1"> Dept of Neurosurgery, Vanderbilt University Medical Center, Nashville TN</nlm:aff><wicri:noCountry code="subfield">Nashville TN</wicri:noCountry></affiliation></author><author><name sortKey="Konrad, Peter E" sort="Konrad, Peter E" uniqKey="Konrad P" first="Peter" last="Konrad">Peter Konrad</name><affiliation><nlm:aff id="A1"> Dept of Neurosurgery, Vanderbilt University Medical Center, Nashville TN</nlm:aff><wicri:noCountry code="subfield">Nashville TN</wicri:noCountry></affiliation></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><idno type="e-ISSN">1531-8257</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">Parkinson’s disease (PD) is a neurodegenerative disorder characterized by progressive loss of dopaminergic cells in the central nervous system, in particular the substantia nigra, resulting in an unrelenting loss of motor and non-motor function. Animal models of PD reveal hyperactive neurons in the subthalamic nucleus (STN) that have increased firing rates and bursting activity compared to controls. Although STN activity has been characterized in advanced stage PD patients, it has not been described in early stage PD patients. Here we present the results of STN neuronal recordings from early stage PD patients (Hoehn and Yahr stage II) enrolled in an ongoing clinical trial compared to recordings from age and sex matched advanced PD patients. STN neurons had a significantly lower firing rate in early versus advanced PD (28.7Hz vs. 36.3Hz; p<0.01). The overall activity of the STN was also significantly lower in early versus late PD, as measured by background neuronal noise (12.4mV vs. 14.0mV; p <0.05). No significant difference was identified between groups in the bursting or variability of neuronal firing in the STN, as measured by a burst index or the interspike interval coefficient of variability. The results suggest that neuronal firing in STN increases with PD progression.</p></div></front></TEI><pmc article-type="research-article" xml:lang="EN"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">8610688</journal-id><journal-id journal-id-type="pubmed-jr-id">5937</journal-id><journal-id journal-id-type="nlm-ta">Mov Disord</journal-id><journal-title>Movement disorders : official journal of the Movement Disorder Society</journal-title><issn pub-type="ppub">0885-3185</issn><issn pub-type="epub">1531-8257</issn></journal-meta><article-meta><article-id pub-id-type="pmid">21542021</article-id><article-id pub-id-type="pmc">3151310</article-id><article-id pub-id-type="doi">10.1002/mds.23708</article-id><article-id pub-id-type="manuscript">NIHMS275511</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Subthalamic Nucleus Neuronal Firing Rate Increases with Parkinson’s Disease Progression</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Remple</surname><given-names>Michael S.</given-names></name><degrees>Ph.D.</degrees><xref rid="A1" ref-type="aff">1</xref></contrib><contrib contrib-type="author"><name><surname>Bradenham</surname><given-names>Courtney H.</given-names></name><degrees>M.D.</degrees><xref rid="A2" ref-type="aff">2</xref></contrib><contrib contrib-type="author"><name><surname>Kao</surname><given-names>C. Chris</given-names></name><degrees>M.D., Ph.D.</degrees><xref rid="A1" ref-type="aff">1</xref></contrib><contrib contrib-type="author"><name><surname>Charles</surname><given-names>P. David</given-names></name><degrees>M.D.</degrees><xref rid="A2" ref-type="aff">2</xref></contrib><contrib contrib-type="author"><name><surname>Neimat</surname><given-names>Joseph S.</given-names></name><degrees>M.D., M.S</degrees><xref rid="A1" ref-type="aff">1</xref></contrib><contrib contrib-type="author"><name><surname>Konrad</surname><given-names>Peter E.</given-names></name><degrees>M.D., Ph.D.</degrees><xref rid="A1" ref-type="aff">1</xref></contrib></contrib-group><aff id="A1"><label>1</label> Dept of Neurosurgery, Vanderbilt University Medical Center, Nashville TN</aff><aff id="A2"><label>2</label> Dept of Neurology, Vanderbilt University Medical Center, Nashville TN</aff><author-notes><corresp id="FN1">Corresponding Author: Peter Konrad, M.D., Ph.D., Associate Professor of Neurological Surgery, Rm T-4224; MCN, Vanderbilt University Medical Center, Nashville, TN 37212, 615.343.9822, fax 615.343.6948, <email>peter.konrad@vanderbilt.edu</email></corresp></author-notes><pub-date pub-type="nihms-submitted"><day>7</day><month>3</month><year>2011</year></pub-date><pub-date pub-type="epub"><day>3</day><month>5</month><year>2011</year></pub-date><pub-date pub-type="ppub"><day>1</day><month>8</month><year>2011</year></pub-date><pub-date pub-type="pmc-release"><day>1</day><month>8</month><year>2012</year></pub-date><volume>26</volume><issue>9</issue><fpage>1657</fpage><lpage>1662</lpage><abstract><p id="P1">Parkinson’s disease (PD) is a neurodegenerative disorder characterized by progressive loss of dopaminergic cells in the central nervous system, in particular the substantia nigra, resulting in an unrelenting loss of motor and non-motor function. Animal models of PD reveal hyperactive neurons in the subthalamic nucleus (STN) that have increased firing rates and bursting activity compared to controls. Although STN activity has been characterized in advanced stage PD patients, it has not been described in early stage PD patients. Here we present the results of STN neuronal recordings from early stage PD patients (Hoehn and Yahr stage II) enrolled in an ongoing clinical trial compared to recordings from age and sex matched advanced PD patients. STN neurons had a significantly lower firing rate in early versus advanced PD (28.7Hz vs. 36.3Hz; p<0.01). The overall activity of the STN was also significantly lower in early versus late PD, as measured by background neuronal noise (12.4mV vs. 14.0mV; p <0.05). No significant difference was identified between groups in the bursting or variability of neuronal firing in the STN, as measured by a burst index or the interspike interval coefficient of variability. The results suggest that neuronal firing in STN increases with PD progression.</p></abstract><kwd-group><kwd>Neurophysiology</kwd><kwd>Neurodegeneration</kwd><kwd>Parkinson’s Disease</kwd><kwd>pathophysiology</kwd><kwd>Subthalamic nucleus</kwd><kwd>rate model</kwd></kwd-group><contract-num rid="RR1">UL1 RR024975-01
||RR</contract-num><contract-sponsor id="RR1">National Center for Research Resources : NCRR</contract-sponsor></article-meta></front></pmc><affiliations><list></list><tree><noCountry><name sortKey="Bradenham, Courtney H" sort="Bradenham, Courtney H" uniqKey="Bradenham C" first="Courtney" last="Bradenham">Courtney Bradenham</name><name sortKey="Charles, P David" sort="Charles, P David" uniqKey="Charles P" first="P" last="Charles">P Charles</name><name sortKey="Kao, C Chris" sort="Kao, C Chris" uniqKey="Kao C" first="C" last="Kao">C Kao</name><name sortKey="Konrad, Peter E" sort="Konrad, Peter E" uniqKey="Konrad P" first="Peter" last="Konrad">Peter Konrad</name><name sortKey="Neimat, Joseph S" sort="Neimat, Joseph S" uniqKey="Neimat J" first="Joseph" last="Neimat">Joseph Neimat</name><name sortKey="Remple, Michael S" sort="Remple, Michael S" uniqKey="Remple M" first="Michael" last="Remple">Michael Remple</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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