Local modulation of striatal glutamate efflux by serotonin 1A receptor stimulation in dyskinetic, hemiparkinsonian rats
Identifieur interne : 000145 ( Pmc/Curation ); précédent : 000144; suivant : 000146Local modulation of striatal glutamate efflux by serotonin 1A receptor stimulation in dyskinetic, hemiparkinsonian rats
Auteurs : Kristin Dupre [États-Unis] ; Corinne Ostock [États-Unis] ; Karen Jaunarajs [États-Unis] ; Thomas Button [États-Unis] ; Lisa Savage [États-Unis] ; William Wolf [États-Unis] ; Christopher Bishop [États-Unis]Source :
- Experimental neurology [ 0014-4886 ] ; 2011.
Abstract
Serotonin 1A receptor (5-HT1AR) agonists reduce both L-DOPA- and D1 receptor (D1R) agonist-mediated dyskinesia, but their anti-dyskinetic mechanism of action is not fully understood. Given that 5-HT1AR stimulation reduces glutamatergic neurotransmission in the dopamine-depleted striatum, 5-HT1AR agonists may diminish dyskinesia in part through modulation of pro-dyskinetic striatal glutamate levels. To test this, rats with unilateral medial forebrain bundle dopamine or sham lesions were primed with L-DOPA (12 mg/kg + benserazide, 15 mg/kg, sc) or the D1R agonist SKF81297 (0.8 mg/kg, sc) until abnormal involuntary movements (AIMs) stabilized. On subsequent test days, rats were treated with vehicle or the 5-HT1AR agonist ±8-OH-DPAT (1.0 mg/kg, sc), followed by L-DOPA or SKF81297, or intrastriatal ±8-OH-DPAT (7.5 or 15 mM), followed by L-DOPA. In some cases, the 5-HT1AR antagonist WAY100635 was employed to determine receptor-specific effects.
Url:
DOI: 10.1016/j.expneurol.2011.02.012
PubMed: 21352823
PubMed Central: 3100430
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type="main">Local modulation of striatal glutamate efflux by serotonin 1A receptor stimulation in dyskinetic, hemiparkinsonian rats</title><author><name sortKey="Dupre, Kristin B" sort="Dupre, Kristin B" uniqKey="Dupre K" first="Kristin" last="Dupre">Kristin Dupre</name><affiliation wicri:level="1"><nlm:aff id="A1">Behavioral Neuroscience Program, Department of Psychology, Binghamton University (State University of New York at Binghamton), Binghamton, NY 13902-6000, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Behavioral Neuroscience Program, Department of Psychology, Binghamton University (State University of New York at Binghamton), Binghamton, NY 13902-6000</wicri:regionArea></affiliation></author><author><name sortKey="Ostock, Corinne Y" sort="Ostock, Corinne Y" uniqKey="Ostock C" first="Corinne" last="Ostock">Corinne Ostock</name><affiliation wicri:level="1"><nlm:aff id="A1">Behavioral Neuroscience Program, Department of Psychology, Binghamton University (State University of New York at Binghamton), Binghamton, NY 13902-6000, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Behavioral Neuroscience Program, Department of Psychology, Binghamton University (State University of New York at Binghamton), Binghamton, NY 13902-6000</wicri:regionArea></affiliation></author><author><name sortKey="Jaunarajs, Karen L Eskow" sort="Jaunarajs, Karen L Eskow" uniqKey="Jaunarajs K" first="Karen" last="Jaunarajs">Karen Jaunarajs</name><affiliation wicri:level="1"><nlm:aff id="A1">Behavioral Neuroscience Program, Department of Psychology, Binghamton University (State University of New York at Binghamton), Binghamton, NY 13902-6000, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Behavioral Neuroscience Program, Department of Psychology, Binghamton University (State University of New York at Binghamton), Binghamton, NY 13902-6000</wicri:regionArea></affiliation></author><author><name sortKey="Button, Thomas" sort="Button, Thomas" uniqKey="Button T" first="Thomas" last="Button">Thomas Button</name><affiliation wicri:level="1"><nlm:aff id="A1">Behavioral Neuroscience Program, Department of Psychology, Binghamton University (State University of New York at Binghamton), Binghamton, NY 13902-6000, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Behavioral Neuroscience Program, Department of Psychology, Binghamton University (State University of New York at Binghamton), Binghamton, NY 13902-6000</wicri:regionArea></affiliation></author><author><name sortKey="Savage, Lisa M" sort="Savage, Lisa M" uniqKey="Savage L" first="Lisa" last="Savage">Lisa Savage</name><affiliation wicri:level="1"><nlm:aff id="A1">Behavioral Neuroscience Program, Department of Psychology, Binghamton University (State University of New York at Binghamton), Binghamton, NY 13902-6000, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Behavioral Neuroscience Program, Department of Psychology, Binghamton University (State University of New York at Binghamton), Binghamton, NY 13902-6000</wicri:regionArea></affiliation></author><author><name sortKey="Wolf, William" sort="Wolf, William" uniqKey="Wolf W" first="William" last="Wolf">William Wolf</name><affiliation wicri:level="2"><nlm:aff id="A2">Research Service, Hines VA Hospital Hines, IL, 60141 and Anatomy & Cell Biology, University of Illinois at Chicago, Chicago, IL 60612</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Illinois</region></placeName><wicri:cityArea>Research Service, Hines VA Hospital Hines, IL, 60141 and Anatomy & Cell Biology, University of Illinois at Chicago, Chicago</wicri:cityArea></affiliation></author><author><name sortKey="Bishop, Christopher" sort="Bishop, Christopher" uniqKey="Bishop C" first="Christopher" last="Bishop">Christopher Bishop</name><affiliation wicri:level="1"><nlm:aff id="A1">Behavioral Neuroscience Program, Department of Psychology, Binghamton University (State University of New York at Binghamton), Binghamton, NY 13902-6000, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Behavioral Neuroscience Program, Department of Psychology, Binghamton University (State University of New York at Binghamton), Binghamton, NY 13902-6000</wicri:regionArea></affiliation></author></analytic><series><title level="j">Experimental neurology</title><idno type="ISSN">0014-4886</idno><idno type="e-ISSN">1090-2430</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">Serotonin 1A receptor (5-HT<sub>1A</sub>R) agonists reduce both L-DOPA- and D1 receptor (D1R) agonist-mediated dyskinesia, but their anti-dyskinetic mechanism of action is not fully understood. Given that 5-HT<sub>1A</sub>R stimulation reduces glutamatergic neurotransmission in the dopamine-depleted striatum, 5-HT<sub>1A</sub>R agonists may diminish dyskinesia in part through modulation of pro-dyskinetic striatal glutamate levels. To test this, rats with unilateral medial forebrain bundle dopamine or sham lesions were primed with L-DOPA (12 mg/kg + benserazide, 15 mg/kg, sc) or the D1R agonist SKF81297 (0.8 mg/kg, sc) until abnormal involuntary movements (AIMs) stabilized. On subsequent test days, rats were treated with vehicle or the 5-HT<sub>1A</sub>R agonist ±8-OH-DPAT (1.0 mg/kg, sc), followed by L-DOPA or SKF81297, or intrastriatal ±8-OH-DPAT (7.5 or 15 mM), followed by L-DOPA. In some cases, the 5-HT<sub>1A</sub>R antagonist WAY100635 was employed to determine receptor-specific effects. <italic>In vivo</italic> microdialysis was used to collect striatal samples for analysis of extracellular glutamate levels during AIMs assessment. Systemic and striatal ±8-OH-DPAT attenuated L-DOPA-induced dyskinesia and striatal glutamate efflux while WAY100635 reversed ±8-OH-DPAT’s effects. Interestingly, systemic ±8-OH-DPAT diminished D1R-mediated AIMs without affecting glutamate. These findings indicate a novel anti-dyskinetic mechanism of action for 5-HT<sub>1A</sub>R agonists with implications for the improved treatment of Parkinson’s disease.</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">0370712</journal-id><journal-id journal-id-type="pubmed-jr-id">3660</journal-id><journal-id journal-id-type="nlm-ta">Exp Neurol</journal-id><journal-title>Experimental neurology</journal-title><issn pub-type="ppub">0014-4886</issn><issn pub-type="epub">1090-2430</issn></journal-meta><article-meta><article-id pub-id-type="pmid">21352823</article-id><article-id pub-id-type="pmc">3100430</article-id><article-id pub-id-type="doi">10.1016/j.expneurol.2011.02.012</article-id><article-id pub-id-type="manuscript">NIHMS276579</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Local modulation of striatal glutamate efflux by serotonin 1A receptor stimulation in dyskinetic, hemiparkinsonian rats</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Dupre</surname><given-names>Kristin B.</given-names></name><xref ref-type="aff" rid="A1">a</xref></contrib><contrib contrib-type="author"><name><surname>Ostock</surname><given-names>Corinne Y.</given-names></name><xref ref-type="aff" rid="A1">a</xref></contrib><contrib contrib-type="author"><name><surname>Jaunarajs</surname><given-names>Karen L. Eskow</given-names></name><xref ref-type="aff" rid="A1">a</xref></contrib><contrib contrib-type="author"><name><surname>Button</surname><given-names>Thomas</given-names></name><xref ref-type="aff" rid="A1">a</xref></contrib><contrib contrib-type="author"><name><surname>Savage</surname><given-names>Lisa M.</given-names></name><xref ref-type="aff" rid="A1">a</xref></contrib><contrib contrib-type="author"><name><surname>Wolf</surname><given-names>William</given-names></name><xref ref-type="aff" rid="A2">b</xref></contrib><contrib contrib-type="author"><name><surname>Bishop</surname><given-names>Christopher</given-names></name><xref ref-type="aff" rid="A1">a</xref></contrib></contrib-group><aff id="A1"><label>a</label>Behavioral Neuroscience Program, Department of Psychology, Binghamton University (State University of New York at Binghamton), Binghamton, NY 13902-6000, USA</aff><aff id="A2"><label>b</label>Research Service, Hines VA Hospital Hines, IL, 60141 and Anatomy & Cell Biology, University of Illinois at Chicago, Chicago, IL 60612</aff><author-notes><corresp id="cor1"><bold>Corresponding Author:</bold> Christopher Bishop, Ph.D., Department of Psychology, Binghamton University – SUNY, 4400 Vestal Parkway East, Binghamton, NY 13902, Phone: 011-1-607-777-3410, Fax: 011-1-607-777-4890, <email>cbishop@binghamton.edu</email></corresp></author-notes><pub-date pub-type="nihms-submitted"><day>28</day><month>2</month><year>2011</year></pub-date><pub-date pub-type="epub"><day>22</day><month>2</month><year>2011</year></pub-date><pub-date pub-type="ppub"><month>6</month><year>2011</year></pub-date><pub-date pub-type="pmc-release"><day>1</day><month>6</month><year>2012</year></pub-date><volume>229</volume><issue>2</issue><fpage>288</fpage><lpage>299</lpage><permissions><copyright-statement>© 2011 Elsevier Inc. All rights reserved.</copyright-statement><copyright-year>2011</copyright-year></permissions><abstract><p id="P1">Serotonin 1A receptor (5-HT<sub>1A</sub>R) agonists reduce both L-DOPA- and D1 receptor (D1R) agonist-mediated dyskinesia, but their anti-dyskinetic mechanism of action is not fully understood. Given that 5-HT<sub>1A</sub>R stimulation reduces glutamatergic neurotransmission in the dopamine-depleted striatum, 5-HT<sub>1A</sub>R agonists may diminish dyskinesia in part through modulation of pro-dyskinetic striatal glutamate levels. To test this, rats with unilateral medial forebrain bundle dopamine or sham lesions were primed with L-DOPA (12 mg/kg + benserazide, 15 mg/kg, sc) or the D1R agonist SKF81297 (0.8 mg/kg, sc) until abnormal involuntary movements (AIMs) stabilized. On subsequent test days, rats were treated with vehicle or the 5-HT<sub>1A</sub>R agonist ±8-OH-DPAT (1.0 mg/kg, sc), followed by L-DOPA or SKF81297, or intrastriatal ±8-OH-DPAT (7.5 or 15 mM), followed by L-DOPA. In some cases, the 5-HT<sub>1A</sub>R antagonist WAY100635 was employed to determine receptor-specific effects. <italic>In vivo</italic> microdialysis was used to collect striatal samples for analysis of extracellular glutamate levels during AIMs assessment. Systemic and striatal ±8-OH-DPAT attenuated L-DOPA-induced dyskinesia and striatal glutamate efflux while WAY100635 reversed ±8-OH-DPAT’s effects. Interestingly, systemic ±8-OH-DPAT diminished D1R-mediated AIMs without affecting glutamate. These findings indicate a novel anti-dyskinetic mechanism of action for 5-HT<sub>1A</sub>R agonists with implications for the improved treatment of Parkinson’s disease.</p></abstract><kwd-group><kwd>5-HT<sub>1A</sub> receptor</kwd><kwd>D1 receptor</kwd><kwd>Glutamate</kwd><kwd>Dyskinesia</kwd><kwd>L-DOPA</kwd><kwd>Parkinson’s disease</kwd></kwd-group><contract-num rid="NS1">R01 NS059600-04
||NS</contract-num><contract-num rid="NS1">R01 NS059600-03
||NS</contract-num><contract-num rid="NS1">R01 NS059600-02
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