BDNF Val66Met Polymorphism Influences Motor System Function in the Human Brain
Identifieur interne : 002679 ( Istex/Corpus ); précédent : 002678; suivant : 002680BDNF Val66Met Polymorphism Influences Motor System Function in the Human Brain
Auteurs : Stephanie A. Mchughen ; Paul F. Rodriguez ; Jeffrey A. Kleim ; Erin D. Kleim ; Laura Marchal Crespo ; Vincent Procaccio ; Steven C. CramerSource :
- Cerebral Cortex [ 1047-3211 ] ; 2009-09-10.
Abstract
Brain-derived neurotrophic factor (BDNF) is important to brain functions such as plasticity and repair. A single nucleotide polymorphism for this growth factor, val66met, is common and associated with decreased activity-dependent BDNF release. The current study evaluated the effects of this polymorphism in relation to human brain motor system function, short-term plasticity, and learning. Functional magnetic resonance imaging (fMRI) scanning during right index finger movement (n24) identified activation in a broad sensorimotor network. However, subjects with the polymorphism showed smaller activation volume within several brain regions as compared with subjects without the polymorphism. Repeat fMRI after 25 min of right index finger training found that the 2 genotype groups modulated brain activation differently. In several brain regions, subjects with the polymorphism showed greater activation volume reduction, whereas subjects without the polymorphism showed greater activation volume expansion. On a driving-based motor learning task (independent cohort, n29), subjects with the polymorphism showed greater error during short-term learning and poorer retention over 4 days, relative to subjects without the polymorphism. The presence of this BDNF polymorphism is associated with differences in brain motor system function, altered short-term plasticity, and greater error in short-term motor learning. The broader implications of these findings are considered.
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DOI: 10.1093/cercor/bhp189
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Kleim</name><affiliation><mods:affiliation>Department of Neuroscience, McKnight Brain Institute, University of Florida, Brain Rehabilitation Research Center, Malcom Randall VA Hospital, Gainesville, FL 32610-0244, USA, Departments of</mods:affiliation></affiliation></author><author><name sortKey="Crespo, Laura Marchal" sort="Crespo, Laura Marchal" uniqKey="Crespo L" first="Laura Marchal" last="Crespo">Laura Marchal Crespo</name><affiliation><mods:affiliation>Mechanical & Aerospace Engineering</mods:affiliation></affiliation></author><author><name sortKey="Procaccio, Vincent" sort="Procaccio, Vincent" uniqKey="Procaccio V" first="Vincent" last="Procaccio">Vincent Procaccio</name><affiliation><mods:affiliation>Pediatrics (Human Genetics Division and Metabolism)</mods:affiliation></affiliation></author><author><name sortKey="Cramer, Steven C" sort="Cramer, Steven C" uniqKey="Cramer S" first="Steven C." last="Cramer">Steven C. Cramer</name><affiliation><mods:affiliation>Department of Anatomy and Neurobiology</mods:affiliation></affiliation><affiliation><mods:affiliation>Neurology, University of California, Irvine, CA 92697, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: scramer@uci.edu</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Cerebral Cortex</title><idno type="ISSN">1047-3211</idno><idno type="eISSN">1460-2199</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2009-09-10">2009-09-10</date><biblScope unit="volume">20</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="1254">1254</biblScope><biblScope unit="page" to="1262">1262</biblScope></imprint><idno type="ISSN">1047-3211</idno></series><idno type="istex">08F1F520873FAB65522D40A8F3E8D727073CB6A0</idno><idno type="DOI">10.1093/cercor/bhp189</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1047-3211</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Brain-derived neurotrophic factor (BDNF) is important to brain functions such as plasticity and repair. A single nucleotide polymorphism for this growth factor, val66met, is common and associated with decreased activity-dependent BDNF release. The current study evaluated the effects of this polymorphism in relation to human brain motor system function, short-term plasticity, and learning. Functional magnetic resonance imaging (fMRI) scanning during right index finger movement (n24) identified activation in a broad sensorimotor network. However, subjects with the polymorphism showed smaller activation volume within several brain regions as compared with subjects without the polymorphism. Repeat fMRI after 25 min of right index finger training found that the 2 genotype groups modulated brain activation differently. In several brain regions, subjects with the polymorphism showed greater activation volume reduction, whereas subjects without the polymorphism showed greater activation volume expansion. On a driving-based motor learning task (independent cohort, n29), subjects with the polymorphism showed greater error during short-term learning and poorer retention over 4 days, relative to subjects without the polymorphism. The presence of this BDNF polymorphism is associated with differences in brain motor system function, altered short-term plasticity, and greater error in short-term motor learning. The broader implications of these findings are considered.</div></front></TEI><istex><corpusName>oup</corpusName><author><json:item><name>Stephanie A. McHughen</name><affiliations><json:string>Department of Anatomy and Neurobiology</json:string></affiliations></json:item><json:item><name>Paul F. Rodriguez</name><affiliations><json:string>Department of Cognitive Science, University of California, Irvine, CA 92697, USA</json:string></affiliations></json:item><json:item><name>Jeffrey A. 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A single nucleotide polymorphism for this growth factor, val66met, is common and associated with decreased activity-dependent BDNF release. The current study evaluated the effects of this polymorphism in relation to human brain motor system function, short-term plasticity, and learning. Functional magnetic resonance imaging (fMRI) scanning during right index finger movement (n24) identified activation in a broad sensorimotor network. However, subjects with the polymorphism showed smaller activation volume within several brain regions as compared with subjects without the polymorphism. Repeat fMRI after 25 min of right index finger training found that the 2 genotype groups modulated brain activation differently. In several brain regions, subjects with the polymorphism showed greater activation volume reduction, whereas subjects without the polymorphism showed greater activation volume expansion. On a driving-based motor learning task (independent cohort, n29), subjects with the polymorphism showed greater error during short-term learning and poorer retention over 4 days, relative to subjects without the polymorphism. The presence of this BDNF polymorphism is associated with differences in brain motor system function, altered short-term plasticity, and greater error in short-term motor learning. 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A single nucleotide polymorphism for this growth factor, val66met, is common and associated with decreased activity-dependent BDNF release. The current study evaluated the effects of this polymorphism in relation to human brain motor system function, short-term plasticity, and learning. Functional magnetic resonance imaging (fMRI) scanning during right index finger movement (n24) identified activation in a broad sensorimotor network. However, subjects with the polymorphism showed smaller activation volume within several brain regions as compared with subjects without the polymorphism. Repeat fMRI after 25 min of right index finger training found that the 2 genotype groups modulated brain activation differently. In several brain regions, subjects with the polymorphism showed greater activation volume reduction, whereas subjects without the polymorphism showed greater activation volume expansion. On a driving-based motor learning task (independent cohort, n29), subjects with the polymorphism showed greater error during short-term learning and poorer retention over 4 days, relative to subjects without the polymorphism. The presence of this BDNF polymorphism is associated with differences in brain motor system function, altered short-term plasticity, and greater error in short-term motor learning. 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Cramer, MD, University of California Irvine Medical Center, 101Š The City Drive South, Building 53, Room 203, Orange, CA 92868-4280, USA. Email: <email>scramer@uci.edu</email>.</corresp></author-notes><pub-date pub-type="epub-ppub"><month>5</month><year>2010</year></pub-date><pub-date pub-type="epub"><day>10</day><month>9</month><year>2009</year></pub-date><volume>20</volume><issue>5</issue><fpage>1254</fpage><lpage>1262</lpage><permissions><copyright-statement>© The Author 2009. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org</copyright-statement><copyright-year>2010</copyright-year></permissions><abstract><p>Brain-derived neurotrophic factor (BDNF) is important to brain functions such as plasticity and repair. A single nucleotide polymorphism for this growth factor, val<sup>66</sup>met, is common and associated with decreased activity-dependent BDNF release. The current study evaluated the effects of this polymorphism in relation to human brain motor system function, short-term plasticity, and learning. Functional magnetic resonance imaging (fMRI) scanning during right index finger movement (<italic>n</italic> = 24) identified activation in a broad sensorimotor network. However, subjects with the polymorphism showed smaller activation volume within several brain regions as compared with subjects without the polymorphism. Repeat fMRI after 25 min of right index finger training found that the 2 genotype groups modulated brain activation differently. In several brain regions, subjects with the polymorphism showed greater activation volume reduction, whereas subjects without the polymorphism showed greater activation volume expansion. On a driving-based motor learning task (independent cohort, <italic>n</italic> = 29), subjects with the polymorphism showed greater error during short-term learning and poorer retention over 4 days, relative to subjects without the polymorphism. The presence of this BDNF polymorphism is associated with differences in brain motor system function, altered short-term plasticity, and greater error in short-term motor learning. The broader implications of these findings are considered.</p></abstract><kwd-group><kwd>cortex</kwd><kwd>fMRI</kwd><kwd>genetics</kwd><kwd>genotype</kwd><kwd>plasticity</kwd></kwd-group></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>BDNF Val66Met Polymorphism Influences Motor System Function in the Human Brain</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>BDNF Val66Met Polymorphism Influences Motor System Function in the Human Brain</title></titleInfo><name type="personal"><namePart type="given">Stephanie A.</namePart><namePart type="family">McHughen</namePart><affiliation>Department of Anatomy and Neurobiology</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Paul F.</namePart><namePart type="family">Rodriguez</namePart><affiliation>Department of Cognitive Science, University of California, Irvine, CA 92697, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jeffrey A.</namePart><namePart type="family">Kleim</namePart><affiliation>Department of Neuroscience, McKnight Brain Institute, University of Florida, Brain Rehabilitation Research Center, Malcom Randall VA Hospital, Gainesville, FL 32610-0244, USA, Departments of</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Erin D.</namePart><namePart type="family">Kleim</namePart><affiliation>Department of Neuroscience, McKnight Brain Institute, University of Florida, Brain Rehabilitation Research Center, Malcom Randall VA Hospital, Gainesville, FL 32610-0244, USA, Departments of</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Laura Marchal</namePart><namePart type="family">Crespo</namePart><affiliation>Mechanical & Aerospace Engineering</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Vincent</namePart><namePart type="family">Procaccio</namePart><affiliation>Pediatrics (Human Genetics Division and Metabolism)</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal" displayLabel="corresp"><namePart type="given">Steven C.</namePart><namePart type="family">Cramer</namePart><affiliation>Department of Anatomy and Neurobiology</affiliation><affiliation>Neurology, University of California, Irvine, CA 92697, USA</affiliation><affiliation>E-mail: scramer@uci.edu</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><subject><topic>Articles</topic></subject><originInfo><publisher>Oxford University Press</publisher><dateIssued encoding="w3cdtf">2009-09-10</dateIssued><dateCreated encoding="w3cdtf">2009-09-10</dateCreated><copyrightDate encoding="w3cdtf">2010</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>Brain-derived neurotrophic factor (BDNF) is important to brain functions such as plasticity and repair. A single nucleotide polymorphism for this growth factor, val66met, is common and associated with decreased activity-dependent BDNF release. The current study evaluated the effects of this polymorphism in relation to human brain motor system function, short-term plasticity, and learning. Functional magnetic resonance imaging (fMRI) scanning during right index finger movement (n24) identified activation in a broad sensorimotor network. However, subjects with the polymorphism showed smaller activation volume within several brain regions as compared with subjects without the polymorphism. Repeat fMRI after 25 min of right index finger training found that the 2 genotype groups modulated brain activation differently. In several brain regions, subjects with the polymorphism showed greater activation volume reduction, whereas subjects without the polymorphism showed greater activation volume expansion. On a driving-based motor learning task (independent cohort, n29), subjects with the polymorphism showed greater error during short-term learning and poorer retention over 4 days, relative to subjects without the polymorphism. The presence of this BDNF polymorphism is associated with differences in brain motor system function, altered short-term plasticity, and greater error in short-term motor learning. The broader implications of these findings are considered.</abstract><subject><genre>Keywords</genre><topic>cortex</topic><topic>fMRI</topic><topic>genetics</topic><topic>genotype</topic><topic>plasticity</topic></subject><relatedItem type="host"><titleInfo><title>Cerebral Cortex</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">1047-3211</identifier><identifier type="eISSN">1460-2199</identifier><identifier type="PublisherID">cercor</identifier><identifier type="PublisherID-hwp">cercor</identifier><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>20</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>1254</start><end>1262</end></extent></part></relatedItem><identifier type="istex">08F1F520873FAB65522D40A8F3E8D727073CB6A0</identifier><identifier type="DOI">10.1093/cercor/bhp189</identifier><accessCondition type="use and reproduction" contentType="copyright">The Author 2009. 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