Effects of intrastriatal infusion of D2 receptor antisense oligonucleotide on apomorphine‐induced behaviors in the rat
Identifieur interne : 001204 ( Istex/Corpus ); précédent : 001203; suivant : 001205Effects of intrastriatal infusion of D2 receptor antisense oligonucleotide on apomorphine‐induced behaviors in the rat
Auteurs : N. Rajakumar ; L. Laurier ; H. B. Niznik ; A. J. StoesslSource :
- Synapse [ 0887-4476 ] ; 1997-07.
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- KwdEn :
Abstract
An antisense oligonucleotide strategy was employed to specifically deplete postsynaptic striatal D2 receptors in order to determine the possible role of presynaptic D2 autoreceptors in mediating behavioral responses induced by low doses of apomorphine. A phosphorothioate‐modified antisense oligonucleotide complementary to the first 19 bases of the coding region of D2 receptor mRNA, a scrambled sequence comprising the same bases, or saline was infused bilaterally into the striatum of adult rats, twice daily for 2 days via indwelling cannulae. After an interval of 8–12 h, rats were habituated and challenged with high (300 μg/kg; subcutaneous) or low (50 μg/kg; s.c.) doses of apomorphine or its vehicle (0.1% ascorbic acid). Yawning, vacuous chewing mouth movements, hypoexploration, and penile grooming induced by low‐dose apomorphine were unaffected by antisense infusion into the striatum, whereas stereotypic sniffing following high‐dose apomorphine was markedly suppressed. Intrastriatal infusion of antisense resulted in significantly diminished [3H]‐raclopride binding, while binding of [3H]‐SCH 23390 (D1 receptors) and [3H]‐WIN 35428 (dopamine transporter) was unchanged. D2 mRNA levels determined by quantitative in situ hybridization were normal in the striatum and the substantia nigra. Our results confirm that stereotypic sniffing is mediated via postsynaptic D2 receptors in the striatum, and favor the notion that behavioral responses induced by low doses of apomorphine are mediated by presynaptic D2 autoreceptors. Synapse 26:199–208, 1997. © 1997 Wiley‐Liss Inc.
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DOI: 10.1002/(SICI)1098-2396(199707)26:3<199::AID-SYN1>3.0.CO;2-2
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ISTEX:13652741AD58A0B263DA018C162EF3D2BB788452Le document en format XML
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A phosphorothioate‐modified antisense oligonucleotide complementary to the first 19 bases of the coding region of D2 receptor mRNA, a scrambled sequence comprising the same bases, or saline was infused bilaterally into the striatum of adult rats, twice daily for 2 days via indwelling cannulae. After an interval of 8–12 h, rats were habituated and challenged with high (300 μg/kg; subcutaneous) or low (50 μg/kg; s.c.) doses of apomorphine or its vehicle (0.1% ascorbic acid). Yawning, vacuous chewing mouth movements, hypoexploration, and penile grooming induced by low‐dose apomorphine were unaffected by antisense infusion into the striatum, whereas stereotypic sniffing following high‐dose apomorphine was markedly suppressed. Intrastriatal infusion of antisense resulted in significantly diminished [3H]‐raclopride binding, while binding of [3H]‐SCH 23390 (D1 receptors) and [3H]‐WIN 35428 (dopamine transporter) was unchanged. D2 mRNA levels determined by quantitative in situ hybridization were normal in the striatum and the substantia nigra. Our results confirm that stereotypic sniffing is mediated via postsynaptic D2 receptors in the striatum, and favor the notion that behavioral responses induced by low doses of apomorphine are mediated by presynaptic D2 autoreceptors. Synapse 26:199–208, 1997. © 1997 Wiley‐Liss Inc.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>N. Rajakumar</name><affiliations><json:string>Department of Clinical Neurological Sciences, University of Western Ontario, London, Ontario, Canada</json:string><json:string>Department of Psychiatry, University of Western Ontario, London, Ontario, Canada</json:string><json:string>Department of Psychiatry, University Hospital, London, Ontario, Canada, N6A 5A5</json:string></affiliations></json:item><json:item><name>L. 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D2 mRNA levels determined by quantitative in situ hybridization were normal in the striatum and the substantia nigra. Our results confirm that stereotypic sniffing is mediated via postsynaptic D2 receptors in the striatum, and favor the notion that behavioral responses induced by low doses of apomorphine are mediated by presynaptic D2 autoreceptors. 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postsynaptic striatal D2 receptors in order to determine the possible role of presynaptic D2 autoreceptors in mediating behavioral responses induced by low doses of apomorphine. A phosphorothioate‐modified antisense oligonucleotide complementary to the first 19 bases of the coding region of D2 receptor mRNA, a scrambled sequence comprising the same bases, or saline was infused bilaterally into the striatum of adult rats, twice daily for 2 days via indwelling cannulae. After an interval of 8–12 h, rats were habituated and challenged with high (300 μg/kg; subcutaneous) or low (50 μg/kg; s.c.) doses of apomorphine or its vehicle (0.1% ascorbic acid). Yawning, vacuous chewing mouth movements, hypoexploration, and penile grooming induced by low‐dose apomorphine were unaffected by antisense infusion into the striatum, whereas stereotypic sniffing following high‐dose apomorphine was markedly suppressed. Intrastriatal infusion of antisense resulted in significantly diminished [3H]‐raclopride binding, while binding of [3H]‐SCH 23390 (D1 receptors) and [3H]‐WIN 35428 (dopamine transporter) was unchanged. D2 mRNA levels determined by quantitative in situ hybridization were normal in the striatum and the substantia nigra. Our results confirm that stereotypic sniffing is mediated via postsynaptic D2 receptors in the striatum, and favor the notion that behavioral responses induced by low doses of apomorphine are mediated by presynaptic D2 autoreceptors. Synapse 26:199–208, 1997. © 1997 Wiley‐Liss Inc.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>keywords</head><item><term>sniffing</term></item><item><term>yawning</term></item><item><term>mouth movements</term></item><item><term>autoreceptors</term></item><item><term>dopamine</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1996-01-24">Received</change><change when="1996-08-31">Registration</change><change when="1997-07">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api-v5.istex.fr/document/13652741AD58A0B263DA018C162EF3D2BB788452/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" 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xml:id="af4" countryCode="CA" type="organization"><unparsedAffiliation>Clarke Institute of Psychiatry, Toronto, Ontario, Canada</unparsedAffiliation></affiliation><affiliation xml:id="curr1" countryCode="CA"><unparsedAffiliation>Neurodegenerative Disorders Centre, Vancouver Hospital and Health Sciences Centre, Vancouver, British Columbia, Canada</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">sniffing</keyword><keyword xml:id="kwd2">yawning</keyword><keyword xml:id="kwd3">mouth movements</keyword><keyword xml:id="kwd4">autoreceptors</keyword><keyword xml:id="kwd5">dopamine</keyword></keywordGroup><fundingInfo><fundingAgency>Medical Research Council of Canada</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Parkinson Foundation of Canada</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Ontario Mental Health Foundation</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Ontario Ministry of Health Career Scientist Award</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>An antisense oligonucleotide strategy was employed to specifically deplete postsynaptic striatal D<sub>2</sub> receptors in order to determine the possible role of presynaptic D<sub>2</sub> autoreceptors in mediating behavioral responses induced by low doses of apomorphine. A phosphorothioate‐modified antisense oligonucleotide complementary to the first 19 bases of the coding region of D<sub>2</sub> receptor mRNA, a scrambled sequence comprising the same bases, or saline was infused bilaterally into the striatum of adult rats, twice daily for 2 days via indwelling cannulae. After an interval of 8–12 h, rats were habituated and challenged with high (300 μg/kg; subcutaneous) or low (50 μg/kg; s.c.) doses of apomorphine or its vehicle (0.1% ascorbic acid). Yawning, vacuous chewing mouth movements, hypoexploration, and penile grooming induced by low‐dose apomorphine were unaffected by antisense infusion into the striatum, whereas stereotypic sniffing following high‐dose apomorphine was markedly suppressed. Intrastriatal infusion of antisense resulted in significantly diminished [<sup>3</sup>H]‐raclopride binding, while binding of [<sup>3</sup>H]‐SCH 23390 (D<sub>1</sub> receptors) and [<sup>3</sup>H]‐WIN 35428 (dopamine transporter) was unchanged. D<sub>2</sub> mRNA levels determined by quantitative in situ hybridization were normal in the striatum and the substantia nigra. Our results confirm that stereotypic sniffing is mediated via postsynaptic D<sub>2</sub> receptors in the striatum, and favor the notion that behavioral responses induced by low doses of apomorphine are mediated by presynaptic D<sub>2</sub> autoreceptors. Synapse 26:199–208, 1997. © 1997 Wiley‐Liss Inc.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Effects of intrastriatal infusion of D2 receptor antisense oligonucleotide on apomorphine‐induced behaviors in the rat</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Effects of intrastriatal infusion of D2 receptor antisense oligonucleotide on apomorphine‐induced behaviors in the rat</title></titleInfo><name type="personal"><namePart type="given">N.</namePart><namePart type="family">Rajakumar</namePart><affiliation>Department of Clinical Neurological Sciences, University of Western Ontario, London, Ontario, Canada</affiliation><affiliation>Department of Psychiatry, University of Western Ontario, London, Ontario, Canada</affiliation><affiliation>Department of Psychiatry, University Hospital, London, Ontario, Canada, N6A 5A5</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L.</namePart><namePart type="family">Laurier</namePart><affiliation>Lawson Research Institute, University of Western Ontario, London, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H.B.</namePart><namePart type="family">Niznik</namePart><affiliation>Clarke Institute of Psychiatry, Toronto, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.J.</namePart><namePart type="family">Stoessl</namePart><affiliation>Department of Clinical Neurological Sciences, University of Western Ontario, London, Ontario, Canada</affiliation><affiliation>Current Address: Neurodegenerative Disorders Centre, Vancouver Hospital and Health Sciences Centre, Vancouver, British Columbia, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>John Wiley & Sons, Inc.</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">1997-07</dateIssued><dateCaptured encoding="w3cdtf">1996-01-24</dateCaptured><dateValid encoding="w3cdtf">1996-08-31</dateValid><copyrightDate encoding="w3cdtf">1997</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">5</extent><extent unit="references">6</extent></physicalDescription><abstract lang="en">An antisense oligonucleotide strategy was employed to specifically deplete postsynaptic striatal D2 receptors in order to determine the possible role of presynaptic D2 autoreceptors in mediating behavioral responses induced by low doses of apomorphine. A phosphorothioate‐modified antisense oligonucleotide complementary to the first 19 bases of the coding region of D2 receptor mRNA, a scrambled sequence comprising the same bases, or saline was infused bilaterally into the striatum of adult rats, twice daily for 2 days via indwelling cannulae. After an interval of 8–12 h, rats were habituated and challenged with high (300 μg/kg; subcutaneous) or low (50 μg/kg; s.c.) doses of apomorphine or its vehicle (0.1% ascorbic acid). Yawning, vacuous chewing mouth movements, hypoexploration, and penile grooming induced by low‐dose apomorphine were unaffected by antisense infusion into the striatum, whereas stereotypic sniffing following high‐dose apomorphine was markedly suppressed. Intrastriatal infusion of antisense resulted in significantly diminished [3H]‐raclopride binding, while binding of [3H]‐SCH 23390 (D1 receptors) and [3H]‐WIN 35428 (dopamine transporter) was unchanged. D2 mRNA levels determined by quantitative in situ hybridization were normal in the striatum and the substantia nigra. Our results confirm that stereotypic sniffing is mediated via postsynaptic D2 receptors in the striatum, and favor the notion that behavioral responses induced by low doses of apomorphine are mediated by presynaptic D2 autoreceptors. Synapse 26:199–208, 1997. © 1997 Wiley‐Liss Inc.</abstract><note type="funding">Medical Research Council of Canada</note><note type="funding">Parkinson Foundation of Canada</note><note type="funding">Ontario Mental Health Foundation</note><note type="funding">Ontario Ministry of Health Career Scientist Award</note><subject lang="en"><genre>keywords</genre><topic>sniffing</topic><topic>yawning</topic><topic>mouth movements</topic><topic>autoreceptors</topic><topic>dopamine</topic></subject><relatedItem type="host"><titleInfo><title>Synapse</title></titleInfo><titleInfo type="abbreviated"><title>Synapse</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0887-4476</identifier><identifier type="eISSN">1098-2396</identifier><identifier type="DOI">10.1002/(ISSN)1098-2396</identifier><identifier type="PublisherID">SYN</identifier><part><date>1997</date><detail type="volume"><caption>vol.</caption><number>26</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>199</start><end>208</end><total>10</total></extent></part></relatedItem><identifier type="istex">13652741AD58A0B263DA018C162EF3D2BB788452</identifier><identifier type="DOI">10.1002/(SICI)1098-2396(199707)26:3<199::AID-SYN1>3.0.CO;2-2</identifier><identifier type="ArticleID">SYN1</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1997 Wiley‐Liss, Inc.</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>John Wiley & Sons, Inc.</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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