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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Thalamic noradrenaline in Parkinson's disease: deficits suggest role in motor and non-motor symptoms</title><author><name sortKey="Pifl, Christian" sort="Pifl, Christian" uniqKey="Pifl C" first="Christian" last="Pifl">Christian Pifl</name><affiliation><nlm:aff id="A1">Center for Brain Research, Medical University of Vienna, A-1090 Vienna, Austria</nlm:aff></affiliation></author><author><name sortKey="Kish, Stephen J" sort="Kish, Stephen J" uniqKey="Kish S" first="Stephen J." last="Kish">Stephen J. Kish</name><affiliation><nlm:aff id="A2">Human Brain Laboratory, Centre for Addiction and Mental Health, Toronto, M5T 1R8 Ontario, Canada</nlm:aff></affiliation></author><author><name sortKey="Hornykiewicz, Oleh" sort="Hornykiewicz, Oleh" uniqKey="Hornykiewicz O" first="Oleh" last="Hornykiewicz">Oleh Hornykiewicz</name><affiliation><nlm:aff id="A1">Center for Brain Research, Medical University of Vienna, A-1090 Vienna, Austria</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">23038412</idno><idno type="pmc">4533102</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4533102</idno><idno type="RBID">PMC:4533102</idno><idno type="doi">10.1002/mds.25109</idno><date when="2012">2012</date><idno type="wicri:Area/Pmc/Corpus">000829</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000829</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Thalamic noradrenaline in Parkinson's disease: deficits suggest role in motor and non-motor symptoms</title><author><name sortKey="Pifl, Christian" sort="Pifl, Christian" uniqKey="Pifl C" first="Christian" last="Pifl">Christian Pifl</name><affiliation><nlm:aff id="A1">Center for Brain Research, Medical University of Vienna, A-1090 Vienna, Austria</nlm:aff></affiliation></author><author><name sortKey="Kish, Stephen J" sort="Kish, Stephen J" uniqKey="Kish S" first="Stephen J." last="Kish">Stephen J. Kish</name><affiliation><nlm:aff id="A2">Human Brain Laboratory, Centre for Addiction and Mental Health, Toronto, M5T 1R8 Ontario, Canada</nlm:aff></affiliation></author><author><name sortKey="Hornykiewicz, Oleh" sort="Hornykiewicz, Oleh" uniqKey="Hornykiewicz O" first="Oleh" last="Hornykiewicz">Oleh Hornykiewicz</name><affiliation><nlm:aff id="A1">Center for Brain Research, Medical University of Vienna, A-1090 Vienna, Austria</nlm:aff></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="eISSN">1531-8257</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec id="S1"><title>Background</title><p id="P1">The thalamus occupies a pivotal position within the cortico-basal ganglia-cortical circuits. In Parkinson's disease, the thalamus exhibits pathological neuronal discharge patterns, foremost increased bursting and oscillatory activity, which are thought to perturb the faithful transfer of basal ganglia impulse flow to the cortex. Analogous abnormal thalamic discharge patterns develop in animals with experimentally reduced thalamic noradrenaline; conversely, added to thalamic neuronal preparations, noradrenaline exhibits marked anti-oscillatory and anti-bursting activity. Our study is based on this experimentally established link between noradrenaline and the quality of thalamic neuronal discharges.</p></sec><sec id="S2"><title>Methods</title><p id="P2">We analysed fourteen thalamic nuclei from all functionally relevant territories of nine patients with Parkinson's disease and eight controls and measured noradrenaline with high pressure liquid chromatography with electrochemical detection.</p></sec><sec id="S3"><title>Results</title><p id="P3">In Parkinson's disease, noradrenaline was profoundly reduced in all nuclei of the motor (pallidonigral and cerebellar) thalamus (ventroanterior: -86%, p=0.0011; ventrolateral oral: -87%, p=0.0010; ventrolateral caudal: -89%, p=0.0014): Also marked noradrenaline losses, ranging from 68% to 91% of controls, were found in other thalamic territories, including associative, limbic and intralaminar regions; the primary sensory regions were only mildly affected.</p></sec><sec id="S4"><title>Conclusions</title><p id="P4">The marked noradrenergic deafferentiation of the thalamus discloses a strategically located noradrenergic component in the overall pathophysiology of the Parkinson's disease, suggesting a role in the complex mechanisms involved with the genesis of the motor and non-motor symptoms. Our study thus significantly contributes to the knowledge of the extrastriatal non-dopaminergic mechanisms of Parkinson's disease with direct relevance to treatment of this disorder.</p></sec></div></front></TEI><pmc article-type="research-article"><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-id journal-id-type="iso-abbrev">Mov. Disord.</journal-id><journal-title-group><journal-title>Movement disorders : official journal of the Movement Disorder Society</journal-title></journal-title-group><issn pub-type="ppub">0885-3185</issn><issn pub-type="epub">1531-8257</issn></journal-meta><article-meta><article-id pub-id-type="pmid">23038412</article-id><article-id pub-id-type="pmc">4533102</article-id><article-id pub-id-type="doi">10.1002/mds.25109</article-id><article-id pub-id-type="manuscript">NIHMS386661</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Thalamic noradrenaline in Parkinson's disease: deficits suggest role in motor and non-motor symptoms</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Pifl</surname><given-names>Christian</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Kish</surname><given-names>Stephen J.</given-names></name><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Hornykiewicz</surname><given-names>Oleh</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib></contrib-group><aff id="A1"><label>1</label>Center for Brain Research, Medical University of Vienna, A-1090 Vienna, Austria</aff><aff id="A2"><label>2</label>Human Brain Laboratory, Centre for Addiction and Mental Health, Toronto, M5T 1R8 Ontario, Canada</aff><author-notes><corresp id="FN1">Correspondence should be addressed to: Oleh Hornykiewicz, MD, Center for Brain Research, Medical University of Vienna, Spitalgasse 4, A-1090 Vienna, Austria, <email>ingrid.kafka@meduniwien.ac.at</email> (O. Hornykiewicz)</corresp></author-notes><pub-date pub-type="nihms-submitted"><day>21</day><month>3</month><year>2014</year></pub-date><pub-date pub-type="epub"><day>04</day><month>10</month><year>2012</year></pub-date><pub-date pub-type="ppub"><month>11</month><year>2012</year></pub-date><pub-date pub-type="pmc-release"><day>12</day><month>8</month><year>2015</year></pub-date><volume>27</volume><issue>13</issue><fpage>1618</fpage><lpage>1624</lpage><pmc-comment>elocation-id from pubmed: 10.1002/mds.25109</pmc-comment>
<abstract><sec id="S1"><title>Background</title><p id="P1">The thalamus occupies a pivotal position within the cortico-basal ganglia-cortical circuits. In Parkinson's disease, the thalamus exhibits pathological neuronal discharge patterns, foremost increased bursting and oscillatory activity, which are thought to perturb the faithful transfer of basal ganglia impulse flow to the cortex. Analogous abnormal thalamic discharge patterns develop in animals with experimentally reduced thalamic noradrenaline; conversely, added to thalamic neuronal preparations, noradrenaline exhibits marked anti-oscillatory and anti-bursting activity. Our study is based on this experimentally established link between noradrenaline and the quality of thalamic neuronal discharges.</p></sec><sec id="S2"><title>Methods</title><p id="P2">We analysed fourteen thalamic nuclei from all functionally relevant territories of nine patients with Parkinson's disease and eight controls and measured noradrenaline with high pressure liquid chromatography with electrochemical detection.</p></sec><sec id="S3"><title>Results</title><p id="P3">In Parkinson's disease, noradrenaline was profoundly reduced in all nuclei of the motor (pallidonigral and cerebellar) thalamus (ventroanterior: -86%, p=0.0011; ventrolateral oral: -87%, p=0.0010; ventrolateral caudal: -89%, p=0.0014): Also marked noradrenaline losses, ranging from 68% to 91% of controls, were found in other thalamic territories, including associative, limbic and intralaminar regions; the primary sensory regions were only mildly affected.</p></sec><sec id="S4"><title>Conclusions</title><p id="P4">The marked noradrenergic deafferentiation of the thalamus discloses a strategically located noradrenergic component in the overall pathophysiology of the Parkinson's disease, suggesting a role in the complex mechanisms involved with the genesis of the motor and non-motor symptoms. Our study thus significantly contributes to the knowledge of the extrastriatal non-dopaminergic mechanisms of Parkinson's disease with direct relevance to treatment of this disorder.</p></sec></abstract><kwd-group><kwd>noradrenaline</kwd><kwd>Parkinson's disease</kwd><kwd>thalamic nuclei</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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