Local modulation of striatal glutamate efflux by serotonin 1A receptor stimulation in dyskinetic, hemiparkinsonian rats
Identifieur interne : 000128 ( Pmc/Checkpoint ); précédent : 000127; suivant : 000129Local 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
Affiliations:
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<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>
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<journal-id journal-id-type="pubmed-jr-id">3660</journal-id>
<journal-id journal-id-type="nlm-ta">Exp Neurol</journal-id>
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<article-id pub-id-type="manuscript">NIHMS276579</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
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<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>
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<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>
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<pub-date pub-type="nihms-submitted"><day>28</day>
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<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>
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||NS</contract-num>
<contract-sponsor id="NS1">National Institute of Neurological Disorders and Stroke : NINDS</contract-sponsor>
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</front>
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<name sortKey="Button, Thomas" sort="Button, Thomas" uniqKey="Button T" first="Thomas" last="Button">Thomas Button</name>
<name sortKey="Jaunarajs, Karen L Eskow" sort="Jaunarajs, Karen L Eskow" uniqKey="Jaunarajs K" first="Karen" last="Jaunarajs">Karen Jaunarajs</name>
<name sortKey="Ostock, Corinne Y" sort="Ostock, Corinne Y" uniqKey="Ostock C" first="Corinne" last="Ostock">Corinne Ostock</name>
<name sortKey="Savage, Lisa M" sort="Savage, Lisa M" uniqKey="Savage L" first="Lisa" last="Savage">Lisa Savage</name>
<name sortKey="Wolf, William" sort="Wolf, William" uniqKey="Wolf W" first="William" last="Wolf">William Wolf</name>
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