Serotonin 1B receptor stimulation reduces D1 receptor agonist-induced dyskinesia
Dopamine replacement therapy for the treatment of Parkinsonʼs disease leads to deleterious abnormal involuntary movements (AIMs), known as L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia, which parallels enhanced striatal dopamine D1 receptor-mediated signaling. Recent evidence suggests sti...
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description | Dopamine replacement therapy for the treatment of Parkinsonʼs disease leads to deleterious abnormal involuntary movements (AIMs), known as L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia, which parallels enhanced striatal dopamine D1 receptor-mediated signaling. Recent evidence suggests stimulation of striatal serotonin (5-HT) 1B receptors may reduce D1-mediated signaling. Given this potential antidyskinetic mechanism, male hemiparkinsonian Sprague–Dawley rats received treatments of D1 receptor agonist, SKF81297, (0.8 mg/kg) or L-DOPA (12 mg/kg, subcutaneous injection). Dyskinetic movements were rated using the AIMs scale. Rats were then administered vehicle (100% dimethyl sulfoxide) or the 5-HT1B receptor agonist, CP94253, (1.5 or 3.0 mg/kg, subcutaneous injection), followed by SKF81297 or L-DOPA and rated for AIMs. Results indicate that CP94253 mitigates both L-DOPA and D1 receptor agonist-induced dyskinesia. These findings suggest that 5-HT1B receptor stimulation directly diminishes D1 receptor-mediated dyskinesia, implicating an important target for the treatment of L-DOPA-induced dyskinesia. |
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Recent evidence suggests stimulation of striatal serotonin (5-HT) 1B receptors may reduce D1-mediated signaling. Given this potential antidyskinetic mechanism, male hemiparkinsonian Sprague–Dawley rats received treatments of D1 receptor agonist, SKF81297, (0.8 mg/kg) or L-DOPA (12 mg/kg, subcutaneous injection). Dyskinetic movements were rated using the AIMs scale. Rats were then administered vehicle (100% dimethyl sulfoxide) or the 5-HT1B receptor agonist, CP94253, (1.5 or 3.0 mg/kg, subcutaneous injection), followed by SKF81297 or L-DOPA and rated for AIMs. Results indicate that CP94253 mitigates both L-DOPA and D1 receptor agonist-induced dyskinesia. These findings suggest that 5-HT1B receptor stimulation directly diminishes D1 receptor-mediated dyskinesia, implicating an important target for the treatment of L-DOPA-induced dyskinesia.</description><identifier>ISSN: 0959-4965</identifier><identifier>EISSN: 1473-558X</identifier><identifier>DOI: 10.1097/WNR.0b013e3283300fd7</identifier><identifier>PMID: 19633584</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins, Inc</publisher><subject>Adrenergic Agents ; Animals ; Benzazepines - toxicity ; Biological and medical sciences ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Dopamine Agonists - toxicity ; Dyskinesia, Drug-Induced - drug therapy ; Levodopa - adverse effects ; Male ; Medical sciences ; Motor Activity - drug effects ; Nervous system (semeiology, syndromes) ; Nervous system as a whole ; Neurology ; Oxidopamine - toxicity ; Parkinsonian Disorders - chemically induced ; Pyridines - pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Dopamine D1 - agonists ; Receptors, Dopamine D1 - metabolism ; Serotonin 5-HT1 Receptor Agonists ; Serotonin Receptor Agonists - pharmacology ; Severity of Illness Index ; Time Factors</subject><ispartof>Neuroreport, 2009-09, Vol.20 (14), p.1265-1269</ispartof><rights>2009 Lippincott Williams & Wilkins, Inc.</rights><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4157-920ff335dcefe7c2df29a1d9567102a44584929952409f0ff6c051c9f0e03adb3</citedby><cites>FETCH-LOGICAL-c4157-920ff335dcefe7c2df29a1d9567102a44584929952409f0ff6c051c9f0e03adb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,778,782,27907,27908</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21945998$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19633584$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Eskow Jaunarajs, Karen L</creatorcontrib><creatorcontrib>Dupre, Kristin B</creatorcontrib><creatorcontrib>Steiniger, Aimee</creatorcontrib><creatorcontrib>Klioueva, Anna</creatorcontrib><creatorcontrib>Moore, Alexander</creatorcontrib><creatorcontrib>Kelly, Catherine</creatorcontrib><creatorcontrib>Bishop, Christopher</creatorcontrib><title>Serotonin 1B receptor stimulation reduces D1 receptor agonist-induced dyskinesia</title><title>Neuroreport</title><addtitle>Neuroreport</addtitle><description>Dopamine replacement therapy for the treatment of Parkinsonʼs disease leads to deleterious abnormal involuntary movements (AIMs), known as L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia, which parallels enhanced striatal dopamine D1 receptor-mediated signaling. Recent evidence suggests stimulation of striatal serotonin (5-HT) 1B receptors may reduce D1-mediated signaling. Given this potential antidyskinetic mechanism, male hemiparkinsonian Sprague–Dawley rats received treatments of D1 receptor agonist, SKF81297, (0.8 mg/kg) or L-DOPA (12 mg/kg, subcutaneous injection). Dyskinetic movements were rated using the AIMs scale. Rats were then administered vehicle (100% dimethyl sulfoxide) or the 5-HT1B receptor agonist, CP94253, (1.5 or 3.0 mg/kg, subcutaneous injection), followed by SKF81297 or L-DOPA and rated for AIMs. Results indicate that CP94253 mitigates both L-DOPA and D1 receptor agonist-induced dyskinesia. These findings suggest that 5-HT1B receptor stimulation directly diminishes D1 receptor-mediated dyskinesia, implicating an important target for the treatment of L-DOPA-induced dyskinesia.</description><subject>Adrenergic Agents</subject><subject>Animals</subject><subject>Benzazepines - toxicity</subject><subject>Biological and medical sciences</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Dopamine Agonists - toxicity</subject><subject>Dyskinesia, Drug-Induced - drug therapy</subject><subject>Levodopa - adverse effects</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Motor Activity - drug effects</subject><subject>Nervous system (semeiology, syndromes)</subject><subject>Nervous system as a whole</subject><subject>Neurology</subject><subject>Oxidopamine - toxicity</subject><subject>Parkinsonian Disorders - chemically induced</subject><subject>Pyridines - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, Dopamine D1 - agonists</subject><subject>Receptors, Dopamine D1 - metabolism</subject><subject>Serotonin 5-HT1 Receptor Agonists</subject><subject>Serotonin Receptor Agonists - pharmacology</subject><subject>Severity of Illness Index</subject><subject>Time Factors</subject><issn>0959-4965</issn><issn>1473-558X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kM1P3DAQxS1UBMvCf4BQLnALzPhjEx9bypeEoCqtyi3y2uPikk22diK0_32NdgUSh55mNO_3Rk-PsUOEUwRdnf26-34Kc0BBgtdCAHhXbbEJykqUStWPn9gEtNKl1DO1y_ZS-gMAGrDeYbuoZ0KoWk7YtweK_dB3oSvwSxHJ0nLoY5GGsBhbM4S-y0c3WkrFV3zXze9sSUMZulfNFW6VnkNHKZh9tu1Nm-hgM6fs5-XFj_Pr8vb-6ub8821pJaqq1By8zxmcJU-V5c5zbdBpNasQuJEyp9Nca8UlaJ_ZmQWFNq8Ewri5mLKT9d9l7P-OlIZmEZKltjUd9WNqOHIUiFUG5Rq0sU8pkm-WMSxMXDUIzWuTTW6y-dhkth1t_o_zBbl306a6DBxvAJOsaX00nQ3pjeOopdK6zly95l76dqCYntvxhWLzRKYdnv6f4R8JfI9y</recordid><startdate>20090923</startdate><enddate>20090923</enddate><creator>Eskow Jaunarajs, Karen L</creator><creator>Dupre, Kristin B</creator><creator>Steiniger, Aimee</creator><creator>Klioueva, Anna</creator><creator>Moore, Alexander</creator><creator>Kelly, Catherine</creator><creator>Bishop, Christopher</creator><general>Lippincott Williams & Wilkins, Inc</general><general>Lippincott Williams & Wilkins</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope></search><sort><creationdate>20090923</creationdate><title>Serotonin 1B receptor stimulation reduces D1 receptor agonist-induced dyskinesia</title><author>Eskow Jaunarajs, Karen L ; Dupre, Kristin B ; Steiniger, Aimee ; Klioueva, Anna ; Moore, Alexander ; Kelly, Catherine ; Bishop, Christopher</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4157-920ff335dcefe7c2df29a1d9567102a44584929952409f0ff6c051c9f0e03adb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Adrenergic Agents</topic><topic>Animals</topic><topic>Benzazepines - toxicity</topic><topic>Biological and medical sciences</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Dopamine Agonists - toxicity</topic><topic>Dyskinesia, Drug-Induced - drug therapy</topic><topic>Levodopa - adverse effects</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Motor Activity - drug effects</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Nervous system as a whole</topic><topic>Neurology</topic><topic>Oxidopamine - toxicity</topic><topic>Parkinsonian Disorders - chemically induced</topic><topic>Pyridines - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Dopamine D1 - agonists</topic><topic>Receptors, Dopamine D1 - metabolism</topic><topic>Serotonin 5-HT1 Receptor Agonists</topic><topic>Serotonin Receptor Agonists - pharmacology</topic><topic>Severity of Illness Index</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Eskow Jaunarajs, Karen L</creatorcontrib><creatorcontrib>Dupre, Kristin B</creatorcontrib><creatorcontrib>Steiniger, Aimee</creatorcontrib><creatorcontrib>Klioueva, Anna</creatorcontrib><creatorcontrib>Moore, Alexander</creatorcontrib><creatorcontrib>Kelly, Catherine</creatorcontrib><creatorcontrib>Bishop, Christopher</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><jtitle>Neuroreport</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Eskow Jaunarajs, Karen L</au><au>Dupre, Kristin B</au><au>Steiniger, Aimee</au><au>Klioueva, Anna</au><au>Moore, Alexander</au><au>Kelly, Catherine</au><au>Bishop, Christopher</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Serotonin 1B receptor stimulation reduces D1 receptor agonist-induced dyskinesia</atitle><jtitle>Neuroreport</jtitle><addtitle>Neuroreport</addtitle><date>2009-09-23</date><risdate>2009</risdate><volume>20</volume><issue>14</issue><spage>1265</spage><epage>1269</epage><pages>1265-1269</pages><issn>0959-4965</issn><eissn>1473-558X</eissn><abstract>Dopamine replacement therapy for the treatment of Parkinsonʼs disease leads to deleterious abnormal involuntary movements (AIMs), known as L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia, which parallels enhanced striatal dopamine D1 receptor-mediated signaling. Recent evidence suggests stimulation of striatal serotonin (5-HT) 1B receptors may reduce D1-mediated signaling. Given this potential antidyskinetic mechanism, male hemiparkinsonian Sprague–Dawley rats received treatments of D1 receptor agonist, SKF81297, (0.8 mg/kg) or L-DOPA (12 mg/kg, subcutaneous injection). Dyskinetic movements were rated using the AIMs scale. Rats were then administered vehicle (100% dimethyl sulfoxide) or the 5-HT1B receptor agonist, CP94253, (1.5 or 3.0 mg/kg, subcutaneous injection), followed by SKF81297 or L-DOPA and rated for AIMs. Results indicate that CP94253 mitigates both L-DOPA and D1 receptor agonist-induced dyskinesia. These findings suggest that 5-HT1B receptor stimulation directly diminishes D1 receptor-mediated dyskinesia, implicating an important target for the treatment of L-DOPA-induced dyskinesia.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins, Inc</pub><pmid>19633584</pmid><doi>10.1097/WNR.0b013e3283300fd7</doi><tpages>5</tpages></addata></record> |
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subjects | Adrenergic Agents Animals Benzazepines - toxicity Biological and medical sciences Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Dopamine Agonists - toxicity Dyskinesia, Drug-Induced - drug therapy Levodopa - adverse effects Male Medical sciences Motor Activity - drug effects Nervous system (semeiology, syndromes) Nervous system as a whole Neurology Oxidopamine - toxicity Parkinsonian Disorders - chemically induced Pyridines - pharmacology Rats Rats, Sprague-Dawley Receptors, Dopamine D1 - agonists Receptors, Dopamine D1 - metabolism Serotonin 5-HT1 Receptor Agonists Serotonin Receptor Agonists - pharmacology Severity of Illness Index Time Factors |
title | Serotonin 1B receptor stimulation reduces D1 receptor agonist-induced dyskinesia |
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