Training-dependent decay in performance produced by the neuroleptic cis(Z)-flupentixol on spatial navigation by rats in a swimming pool
Identifieur interne : 002A09 ( Istex/Corpus ); précédent : 002A08; suivant : 002A10Training-dependent decay in performance produced by the neuroleptic cis(Z)-flupentixol on spatial navigation by rats in a swimming pool
Auteurs : Ian Q. Whishaw ; Guy Mittleman ; John L. EvendenSource :
- Pharmacology, Biochemistry and Behavior [ 0091-3057 ] ; 1989.
Abstract
Rats were trained on place or cue spatial navigation tasks in a swimming pool and then given the neuroleptic, alpha-flupentixol. Initial experiments showed that regardless of testing schedule, including blocks of trials given concurrently or separated by 7 or 30 days, drugged rats showed a trial-by-trial decay in latency and accuracy of responding although they continued to swim. The rate of decay increased with increases in drug dosage. Further experiments showed that: 1) Performance decay was specifically related to conditioned components of the test environment. Animals required to swim in a different test, or to struggle, showed less decay than rats exposed to the test platform only or required to perform all aspects of the task. 2) Decay was not due to nonspecific effects of neuroleptic treatment because rats injected and replaced in their home cage, and then subsequently reinjected and tested performed like rats treated and tested for the first time. 3) A trial-dependent decay of performance was also obtained in hippocampectomized and decorticate rats, suggesting that at least part of the major action of the drug is on subcortical systems. The results are discussed with respect to hypotheses of neuroleptic action and with respect to their possible relevance to experience-dependent changes in animal analogues of Parkinson's disease. Finally, it is suggested that behavior may be organized in subsystems, which when active, become selectively sensitive to neuroleptics.
Url:
DOI: 10.1016/0091-3057(89)90236-0
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Whishaw</name><affiliation><mods:affiliation>Department of Psychology, University of Lethbridge Lethbridge, Alberta, Canada, T1K 3M4</mods:affiliation></affiliation></author><author><name sortKey="Mittleman, Guy" sort="Mittleman, Guy" uniqKey="Mittleman G" first="Guy" last="Mittleman">Guy Mittleman</name><affiliation><mods:affiliation>Department of Experimental Psychology, University of Cambridge Downing Street, Cambridge, England, CB2 3EB, UK</mods:affiliation></affiliation></author><author><name sortKey="Evenden, John L" sort="Evenden, John L" uniqKey="Evenden J" first="John L." last="Evenden">John L. 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Initial experiments showed that regardless of testing schedule, including blocks of trials given concurrently or separated by 7 or 30 days, drugged rats showed a trial-by-trial decay in latency and accuracy of responding although they continued to swim. The rate of decay increased with increases in drug dosage. Further experiments showed that: 1) Performance decay was specifically related to conditioned components of the test environment. Animals required to swim in a different test, or to struggle, showed less decay than rats exposed to the test platform only or required to perform all aspects of the task. 2) Decay was not due to nonspecific effects of neuroleptic treatment because rats injected and replaced in their home cage, and then subsequently reinjected and tested performed like rats treated and tested for the first time. 3) A trial-dependent decay of performance was also obtained in hippocampectomized and decorticate rats, suggesting that at least part of the major action of the drug is on subcortical systems. The results are discussed with respect to hypotheses of neuroleptic action and with respect to their possible relevance to experience-dependent changes in animal analogues of Parkinson's disease. 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Initial experiments showed that regardless of testing schedule, including blocks of trials given concurrently or separated by 7 or 30 days, drugged rats showed a trial-by-trial decay in latency and accuracy of responding although they continued to swim. The rate of decay increased with increases in drug dosage. Further experiments showed that: 1) Performance decay was specifically related to conditioned components of the test environment. Animals required to swim in a different test, or to struggle, showed less decay than rats exposed to the test platform only or required to perform all aspects of the task. 2) Decay was not due to nonspecific effects of neuroleptic treatment because rats injected and replaced in their home cage, and then subsequently reinjected and tested performed like rats treated and tested for the first time. 3) A trial-dependent decay of performance was also obtained in hippocampectomized and decorticate rats, suggesting that at least part of the major action of the drug is on subcortical systems. The results are discussed with respect to hypotheses of neuroleptic action and with respect to their possible relevance to experience-dependent changes in animal analogues of Parkinson's disease. Finally, it is suggested that behavior may be organized in subsystems, which when active, become selectively sensitive to neuroleptics.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>Alpha-flupentixol and spatial navigation</term></item><item><term>Decortication and neuroleptics</term></item><item><term>Hippocampectomy and neuroleptics</term></item><item><term>Neuroleptics and extinction</term></item><item><term>Neuroleptics and spatial navigation</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1989">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/62501850DF2FD6FEC95A7812BC01381B5DF57D40/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>PBB</jid><aid>89902360</aid><ce:pii>0091-3057(89)90236-0</ce:pii><ce:doi>10.1016/0091-3057(89)90236-0</ce:doi><ce:copyright type="unknown" year="1989"></ce:copyright></item-info><head><ce:title>Training-dependent decay in performance produced by the neuroleptic cis(Z)-flupentixol on spatial navigation by rats in a swimming pool</ce:title><ce:author-group><ce:author><ce:given-name>Ian Q.</ce:given-name><ce:surname>Whishaw</ce:surname></ce:author><ce:affiliation><ce:textfn>Department of Psychology, University of Lethbridge Lethbridge, Alberta, Canada, T1K 3M4</ce:textfn></ce:affiliation></ce:author-group><ce:author-group><ce:author><ce:given-name>Guy</ce:given-name><ce:surname>Mittleman</ce:surname></ce:author><ce:author><ce:given-name>John L.</ce:given-name><ce:surname>Evenden</ce:surname></ce:author><ce:affiliation><ce:textfn>Department of Experimental Psychology, University of Cambridge Downing Street, Cambridge, England, CB2 3EB, UK</ce:textfn></ce:affiliation></ce:author-group><ce:date-received day="14" month="12" year="1987"></ce:date-received><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Rats were trained on place or cue spatial navigation tasks in a swimming pool and then given the neuroleptic, alpha-flupentixol. Initial experiments showed that regardless of testing schedule, including blocks of trials given concurrently or separated by 7 or 30 days, drugged rats showed a trial-by-trial decay in latency and accuracy of responding although they continued to swim. The rate of decay increased with increases in drug dosage. Further experiments showed that: 1) Performance decay was specifically related to conditioned components of the test environment. Animals required to swim in a different test, or to struggle, showed less decay than rats exposed to the test platform only or required to perform all aspects of the task. 2) Decay was not due to nonspecific effects of neuroleptic treatment because rats injected and replaced in their home cage, and then subsequently reinjected and tested performed like rats treated and tested for the first time. 3) A trial-dependent decay of performance was also obtained in hippocampectomized and decorticate rats, suggesting that at least part of the major action of the drug is on subcortical systems. The results are discussed with respect to hypotheses of neuroleptic action and with respect to their possible relevance to experience-dependent changes in animal analogues of Parkinson's disease. Finally, it is suggested that behavior may be organized in subsystems, which when active, become selectively sensitive to neuroleptics.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Alpha-flupentixol and spatial navigation</ce:text></ce:keyword><ce:keyword><ce:text>Decortication and neuroleptics</ce:text></ce:keyword><ce:keyword><ce:text>Hippocampectomy and neuroleptics</ce:text></ce:keyword><ce:keyword><ce:text>Neuroleptics and extinction</ce:text></ce:keyword><ce:keyword><ce:text>Neuroleptics and spatial navigation</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Training-dependent decay in performance produced by the neuroleptic cis(Z)-flupentixol on spatial navigation by rats in a swimming pool</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Training-dependent decay in performance produced by the neuroleptic cis(Z)-flupentixol on spatial navigation by rats in a swimming pool</title></titleInfo><name type="personal"><namePart type="given">Ian Q.</namePart><namePart type="family">Whishaw</namePart><affiliation>Department of Psychology, University of Lethbridge Lethbridge, Alberta, Canada, T1K 3M4</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Guy</namePart><namePart type="family">Mittleman</namePart><affiliation>Department of Experimental Psychology, University of Cambridge Downing Street, Cambridge, England, CB2 3EB, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">John L.</namePart><namePart type="family">Evenden</namePart><affiliation>Department of Experimental Psychology, University of Cambridge Downing Street, Cambridge, England, CB2 3EB, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1989</dateIssued><copyrightDate encoding="w3cdtf">1989</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Rats were trained on place or cue spatial navigation tasks in a swimming pool and then given the neuroleptic, alpha-flupentixol. Initial experiments showed that regardless of testing schedule, including blocks of trials given concurrently or separated by 7 or 30 days, drugged rats showed a trial-by-trial decay in latency and accuracy of responding although they continued to swim. The rate of decay increased with increases in drug dosage. Further experiments showed that: 1) Performance decay was specifically related to conditioned components of the test environment. Animals required to swim in a different test, or to struggle, showed less decay than rats exposed to the test platform only or required to perform all aspects of the task. 2) Decay was not due to nonspecific effects of neuroleptic treatment because rats injected and replaced in their home cage, and then subsequently reinjected and tested performed like rats treated and tested for the first time. 3) A trial-dependent decay of performance was also obtained in hippocampectomized and decorticate rats, suggesting that at least part of the major action of the drug is on subcortical systems. The results are discussed with respect to hypotheses of neuroleptic action and with respect to their possible relevance to experience-dependent changes in animal analogues of Parkinson's disease. Finally, it is suggested that behavior may be organized in subsystems, which when active, become selectively sensitive to neuroleptics.</abstract><subject><genre>Keywords</genre><topic>Alpha-flupentixol and spatial navigation</topic><topic>Decortication and neuroleptics</topic><topic>Hippocampectomy and neuroleptics</topic><topic>Neuroleptics and extinction</topic><topic>Neuroleptics and spatial navigation</topic></subject><relatedItem type="host"><titleInfo><title>Pharmacology, Biochemistry and Behavior</title></titleInfo><titleInfo type="abbreviated"><title>PBB</title></titleInfo><genre type="journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">198901</dateIssued></originInfo><identifier type="ISSN">0091-3057</identifier><identifier type="PII">S0091-3057(00)X0163-3</identifier><part><date>198901</date><detail type="volume"><number>32</number><caption>vol.</caption></detail><detail type="issue"><number>1</number><caption>no.</caption></detail><extent unit="issue pages"><start>1</start><end>366</end></extent><extent unit="pages"><start>211</start><end>220</end></extent></part></relatedItem><identifier type="istex">62501850DF2FD6FEC95A7812BC01381B5DF57D40</identifier><identifier type="DOI">10.1016/0091-3057(89)90236-0</identifier><identifier type="PII">0091-3057(89)90236-0</identifier><recordInfo><recordContentSource>ELSEVIER</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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