Nicotine stimulates dendritic arborization in motor cortex and improves concurrent motor skill but impairs subsequent motor learning
Identifieur interne : 001771 ( Istex/Corpus ); précédent : 001770; suivant : 001772Nicotine stimulates dendritic arborization in motor cortex and improves concurrent motor skill but impairs subsequent motor learning
Auteurs : Claudia L. R. Gonzalez ; Omar A. Gharbawie ; Ian Q. Whishaw ; Bryan KolbSource :
- Synapse [ 0887-4476 ] ; 2005-03.
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Abstract
The effect of the premature commitment of neurons to exuberant growth by nicotine on concurrent and subsequent learning is unknown and was the focus of the present study. Animals were trained on a tray reaching for food task (where lots of pieces of chicken feed were available) for 3 weeks before they received two daily injections of nicotine (0.3 mg/kg) or 0.9% saline for 12 days. Measures of tray‐reaching performance were obtained before the administration of nicotine and every other week for a total of 7 weeks. Starting on week 8, animals were given a novel motor skill problem that required them to learn to use a forepaw to reach through a slot in a cage for single food pellets located on an external shelf. Pyramidal cells in the forelimb area of both hemispheres were then examined for dendritic length and branching using a Golgi‐Cox procedure. Animals treated with saline displayed excellent performance in both reaching tasks and an increase in neuronal branching in Layer V pyramidal cells in the motor cortex contralateral to the reaching paw. In contrast, animals treated with nicotine showed bilateral increases in neuronal branching. Behavioral results showed that nicotine improved forelimb use in the concurrently administered tray‐reaching task, but severely degraded quantitative and qualitative scores of skilled forelimb use in the subsequently administered single‐pellet reaching task. The results suggest that plasticity coincidence with skilled training is essential to skilled motor learning, but this expenditure can impair subsequent learning. Synapse 55:183–191, 2005. © 2005 Wiley‐Liss, Inc.
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DOI: 10.1002/syn.20106
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Animals were trained on a tray reaching for food task (where lots of pieces of chicken feed were available) for 3 weeks before they received two daily injections of nicotine (0.3 mg/kg) or 0.9% saline for 12 days. Measures of tray‐reaching performance were obtained before the administration of nicotine and every other week for a total of 7 weeks. Starting on week 8, animals were given a novel motor skill problem that required them to learn to use a forepaw to reach through a slot in a cage for single food pellets located on an external shelf. Pyramidal cells in the forelimb area of both hemispheres were then examined for dendritic length and branching using a Golgi‐Cox procedure. Animals treated with saline displayed excellent performance in both reaching tasks and an increase in neuronal branching in Layer V pyramidal cells in the motor cortex contralateral to the reaching paw. In contrast, animals treated with nicotine showed bilateral increases in neuronal branching. Behavioral results showed that nicotine improved forelimb use in the concurrently administered tray‐reaching task, but severely degraded quantitative and qualitative scores of skilled forelimb use in the subsequently administered single‐pellet reaching task. The results suggest that plasticity coincidence with skilled training is essential to skilled motor learning, but this expenditure can impair subsequent learning. Synapse 55:183–191, 2005. © 2005 Wiley‐Liss, Inc.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Claudia L.R. Gonzalez</name><affiliations><json:string>Department of Psychology and Neuroscience, Canadian Centre for Behavioral Neuroscience, University of Lethbridge, Lethbridge, Alberta, T1K 3M4, Canada</json:string><json:string>Canadian Centre for Behavioral Neuroscience, University of Lethbridge, 4401 University Dr., Lethbridge, AB, T1K 3M4, Canada</json:string></affiliations></json:item><json:item><name>Omar A. 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Animals were trained on a tray reaching for food task (where lots of pieces of chicken feed were available) for 3 weeks before they received two daily injections of nicotine (0.3 mg/kg) or 0.9% saline for 12 days. Measures of tray‐reaching performance were obtained before the administration of nicotine and every other week for a total of 7 weeks. Starting on week 8, animals were given a novel motor skill problem that required them to learn to use a forepaw to reach through a slot in a cage for single food pellets located on an external shelf. Pyramidal cells in the forelimb area of both hemispheres were then examined for dendritic length and branching using a Golgi‐Cox procedure. Animals treated with saline displayed excellent performance in both reaching tasks and an increase in neuronal branching in Layer V pyramidal cells in the motor cortex contralateral to the reaching paw. In contrast, animals treated with nicotine showed bilateral increases in neuronal branching. Behavioral results showed that nicotine improved forelimb use in the concurrently administered tray‐reaching task, but severely degraded quantitative and qualitative scores of skilled forelimb use in the subsequently administered single‐pellet reaching task. The results suggest that plasticity coincidence with skilled training is essential to skilled motor learning, but this expenditure can impair subsequent learning. 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Research</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The effect of the premature commitment of neurons to exuberant growth by nicotine on concurrent and subsequent learning is unknown and was the focus of the present study. Animals were trained on a tray reaching for food task (where lots of pieces of chicken feed were available) for 3 weeks before they received two daily injections of nicotine (0.3 mg/kg) or 0.9% saline for 12 days. Measures of tray‐reaching performance were obtained before the administration of nicotine and every other week for a total of 7 weeks. Starting on week 8, animals were given a novel motor skill problem that required them to learn to use a forepaw to reach through a slot in a cage for single food pellets located on an external shelf. Pyramidal cells in the forelimb area of both hemispheres were then examined for dendritic length and branching using a Golgi‐Cox procedure. Animals treated with saline displayed excellent performance in both reaching tasks and an increase in neuronal branching in Layer V pyramidal cells in the motor cortex contralateral to the reaching paw. In contrast, animals treated with nicotine showed bilateral increases in neuronal branching. Behavioral results showed that nicotine improved forelimb use in the concurrently administered tray‐reaching task, but severely degraded quantitative and qualitative scores of skilled forelimb use in the subsequently administered single‐pellet reaching task. The results suggest that plasticity coincidence with skilled training is essential to skilled motor learning, but this expenditure can impair subsequent learning. Synapse 55:183–191, 2005. © 2005 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Nicotine stimulates dendritic arborization in motor cortex and improves concurrent motor skill but impairs subsequent motor learning</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Effects of Nicotine on Skilled Reaching</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Nicotine stimulates dendritic arborization in motor cortex and improves concurrent motor skill but impairs subsequent motor learning</title></titleInfo><name type="personal"><namePart type="given">Claudia L.R.</namePart><namePart type="family">Gonzalez</namePart><affiliation>Department of Psychology and Neuroscience, Canadian Centre for Behavioral Neuroscience, University of Lethbridge, Lethbridge, Alberta, T1K 3M4, Canada</affiliation><affiliation>Canadian Centre for Behavioral Neuroscience, University of Lethbridge, 4401 University Dr., Lethbridge, AB, T1K 3M4, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Omar A.</namePart><namePart type="family">Gharbawie</namePart><affiliation>Department of Psychology and Neuroscience, Canadian Centre for Behavioral Neuroscience, University of Lethbridge, Lethbridge, Alberta, T1K 3M4, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ian Q.</namePart><namePart type="family">Whishaw</namePart><affiliation>Department of Psychology and Neuroscience, Canadian Centre for Behavioral Neuroscience, University of Lethbridge, Lethbridge, Alberta, T1K 3M4, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Bryan</namePart><namePart type="family">Kolb</namePart><affiliation>Department of Psychology and Neuroscience, Canadian Centre for Behavioral Neuroscience, University of Lethbridge, Lethbridge, Alberta, T1K 3M4, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2005-03</dateIssued><dateCaptured encoding="w3cdtf">2004-08-30</dateCaptured><dateValid encoding="w3cdtf">2004-11-05</dateValid><copyrightDate encoding="w3cdtf">2005</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">7</extent><extent unit="references">39</extent><extent unit="words">6900</extent></physicalDescription><abstract lang="en">The effect of the premature commitment of neurons to exuberant growth by nicotine on concurrent and subsequent learning is unknown and was the focus of the present study. Animals were trained on a tray reaching for food task (where lots of pieces of chicken feed were available) for 3 weeks before they received two daily injections of nicotine (0.3 mg/kg) or 0.9% saline for 12 days. Measures of tray‐reaching performance were obtained before the administration of nicotine and every other week for a total of 7 weeks. Starting on week 8, animals were given a novel motor skill problem that required them to learn to use a forepaw to reach through a slot in a cage for single food pellets located on an external shelf. Pyramidal cells in the forelimb area of both hemispheres were then examined for dendritic length and branching using a Golgi‐Cox procedure. Animals treated with saline displayed excellent performance in both reaching tasks and an increase in neuronal branching in Layer V pyramidal cells in the motor cortex contralateral to the reaching paw. In contrast, animals treated with nicotine showed bilateral increases in neuronal branching. Behavioral results showed that nicotine improved forelimb use in the concurrently administered tray‐reaching task, but severely degraded quantitative and qualitative scores of skilled forelimb use in the subsequently administered single‐pellet reaching task. The results suggest that plasticity coincidence with skilled training is essential to skilled motor learning, but this expenditure can impair subsequent learning. Synapse 55:183–191, 2005. © 2005 Wiley‐Liss, Inc.</abstract><note type="funding">Canadian Stroke Network</note><note type="funding">Alberta Heritage Foundation for Medical Research</note><subject lang="en"><genre>keywords</genre><topic>brain plasticity</topic><topic>Golgi‐Cox</topic><topic>Long‐Evans rat</topic><topic>nicotine</topic><topic>sensorimotor cortex</topic><topic>skilled reaching</topic></subject><relatedItem type="host"><titleInfo><title>Synapse</title></titleInfo><titleInfo type="abbreviated"><title>Synapse</title></titleInfo><genre type="journal">journal</genre><subject><genre>article-category</genre><topic>Research Article</topic></subject><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>2005</date><detail type="volume"><caption>vol.</caption><number>55</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>183</start><end>191</end><total>9</total></extent></part></relatedItem><identifier type="istex">7BDEAB65E4FD81C2D6F7B9A19197576D13BC60CE</identifier><identifier type="DOI">10.1002/syn.20106</identifier><identifier type="ArticleID">SYN20106</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2005 Wiley‐Liss, Inc.</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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