Life stress in adolescence predicts early adult reward-related brain function and alcohol dependence.
Identifieur interne : 000482 ( PubMed/Corpus ); précédent : 000481; suivant : 000483Life stress in adolescence predicts early adult reward-related brain function and alcohol dependence.
Auteurs : Melynda D. Casement ; Daniel S. Shaw ; Stephanie L. Sitnick ; Samuel C. Musselman ; Erika E. ForbesSource :
- Social cognitive and affective neuroscience [ 1749-5024 ] ; 2015.
English descriptors
- KwdEn :
- Adolescent, Aging (psychology), Alcoholism (physiopathology), Alcoholism (psychology), Anticipation, Psychological, Brain (physiopathology), Child, Child, Preschool, Female, Humans, Infant, Longitudinal Studies, Magnetic Resonance Imaging, Male, Motivation, Nerve Net (physiopathology), Prefrontal Cortex (pathology), Prefrontal Cortex (physiopathology), Psychomotor Performance, Reward, Stress, Psychological (psychology), Tobacco Use (psychology), Young Adult.
- MESH :
- pathology : Prefrontal Cortex.
- physiopathology : Alcoholism, Brain, Nerve Net, Prefrontal Cortex.
- psychology : Aging, Alcoholism, Stress, Psychological, Tobacco Use.
- Adolescent, Anticipation, Psychological, Child, Child, Preschool, Female, Humans, Infant, Longitudinal Studies, Magnetic Resonance Imaging, Male, Motivation, Psychomotor Performance, Reward, Young Adult.
Abstract
Stressful life events increase vulnerability to problematic alcohol use, and they may do this by disrupting reward-related neural circuitry. This is particularly relevant for adolescents because alcohol use rises sharply after mid-adolescence and alcohol abuse peaks at age 20. Adolescents also report more stressors compared with children, and neural reward circuitry may be especially vulnerable to stressors during adolescence because of prefrontal cortex remodeling. Using a large sample of male participants in a longitudinal functional magnetic resonance imaging study (N = 157), we evaluated whether cumulative stressful life events between the ages of 15 and 18 were associated with reward-related brain function and problematic alcohol use at age 20 years. Higher cumulative stressful life events during adolescence were associated with decreased response in the medial prefrontal cortex (mPFC) during monetary reward anticipation and following the receipt of monetary rewards. Stress-related decreases in mPFC response during reward anticipation and following rewarding outcomes were associated with the severity of alcohol dependence. Furthermore, mPFC response mediated the association between stressful life events and later symptoms of alcohol dependence. These data are consistent with neurobiological models of addiction that propose that stressors during adolescence increase risk for problematic alcohol use by disrupting reward circuit function.
DOI: 10.1093/scan/nsu061
PubMed: 24795442
Links to Exploration step
pubmed:24795442Le document en format XML
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Shaw</name><affiliation><nlm:affiliation>Department of Psychiatry, Department of Psychology, Department of Pediatrics, and Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, PA, USA 15213.</nlm:affiliation></affiliation></author><author><name sortKey="Sitnick, Stephanie L" sort="Sitnick, Stephanie L" uniqKey="Sitnick S" first="Stephanie L" last="Sitnick">Stephanie L. Sitnick</name><affiliation><nlm:affiliation>Department of Psychiatry, Department of Psychology, Department of Pediatrics, and Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, PA, USA 15213.</nlm:affiliation></affiliation></author><author><name sortKey="Musselman, Samuel C" sort="Musselman, Samuel C" uniqKey="Musselman S" first="Samuel C" last="Musselman">Samuel C. 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Forbes</name><affiliation><nlm:affiliation>Department of Psychiatry, Department of Psychology, Department of Pediatrics, and Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, PA, USA 15213 Department of Psychiatry, Department of Psychology, Department of Pediatrics, and Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, PA, USA 15213 Department of Psychiatry, Department of Psychology, Department of Pediatrics, and Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, PA, USA 15213 Department of Psychiatry, Department of Psychology, Department of Pediatrics, and Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, PA, USA 15213.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2015">2015</date><idno type="RBID">pubmed:24795442</idno><idno type="pmid">24795442</idno><idno type="doi">10.1093/scan/nsu061</idno><idno type="wicri:Area/PubMed/Corpus">000482</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000482</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Life stress in adolescence predicts early adult reward-related brain function and alcohol dependence.</title><author><name sortKey="Casement, Melynda D" sort="Casement, Melynda D" uniqKey="Casement M" first="Melynda D" last="Casement">Melynda D. Casement</name><affiliation><nlm:affiliation>Department of Psychiatry, Department of Psychology, Department of Pediatrics, and Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, PA, USA 15213 Department of Psychiatry, Department of Psychology, Department of Pediatrics, and Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, PA, USA 15213 forbese@upmc.edu.</nlm:affiliation></affiliation></author><author><name sortKey="Shaw, Daniel S" sort="Shaw, Daniel S" uniqKey="Shaw D" first="Daniel S" last="Shaw">Daniel S. Shaw</name><affiliation><nlm:affiliation>Department of Psychiatry, Department of Psychology, Department of Pediatrics, and Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, PA, USA 15213.</nlm:affiliation></affiliation></author><author><name sortKey="Sitnick, Stephanie L" sort="Sitnick, Stephanie L" uniqKey="Sitnick S" first="Stephanie L" last="Sitnick">Stephanie L. Sitnick</name><affiliation><nlm:affiliation>Department of Psychiatry, Department of Psychology, Department of Pediatrics, and Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, PA, USA 15213.</nlm:affiliation></affiliation></author><author><name sortKey="Musselman, Samuel C" sort="Musselman, Samuel C" uniqKey="Musselman S" first="Samuel C" last="Musselman">Samuel C. Musselman</name><affiliation><nlm:affiliation>Department of Psychiatry, Department of Psychology, Department of Pediatrics, and Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, PA, USA 15213.</nlm:affiliation></affiliation></author><author><name sortKey="Forbes, Erika E" sort="Forbes, Erika E" uniqKey="Forbes E" first="Erika E" last="Forbes">Erika E. Forbes</name><affiliation><nlm:affiliation>Department of Psychiatry, Department of Psychology, Department of Pediatrics, and Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, PA, USA 15213 Department of Psychiatry, Department of Psychology, Department of Pediatrics, and Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, PA, USA 15213 Department of Psychiatry, Department of Psychology, Department of Pediatrics, and Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, PA, USA 15213 Department of Psychiatry, Department of Psychology, Department of Pediatrics, and Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, PA, USA 15213.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Social cognitive and affective neuroscience</title><idno type="eISSN">1749-5024</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adolescent</term><term>Aging (psychology)</term><term>Alcoholism (physiopathology)</term><term>Alcoholism (psychology)</term><term>Anticipation, Psychological</term><term>Brain (physiopathology)</term><term>Child</term><term>Child, Preschool</term><term>Female</term><term>Humans</term><term>Infant</term><term>Longitudinal Studies</term><term>Magnetic Resonance Imaging</term><term>Male</term><term>Motivation</term><term>Nerve Net (physiopathology)</term><term>Prefrontal Cortex (pathology)</term><term>Prefrontal Cortex (physiopathology)</term><term>Psychomotor Performance</term><term>Reward</term><term>Stress, Psychological (psychology)</term><term>Tobacco Use (psychology)</term><term>Young Adult</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Prefrontal Cortex</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Alcoholism</term><term>Brain</term><term>Nerve Net</term><term>Prefrontal Cortex</term></keywords><keywords scheme="MESH" qualifier="psychology" xml:lang="en"><term>Aging</term><term>Alcoholism</term><term>Stress, Psychological</term><term>Tobacco Use</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adolescent</term><term>Anticipation, Psychological</term><term>Child</term><term>Child, Preschool</term><term>Female</term><term>Humans</term><term>Infant</term><term>Longitudinal Studies</term><term>Magnetic Resonance Imaging</term><term>Male</term><term>Motivation</term><term>Psychomotor Performance</term><term>Reward</term><term>Young Adult</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Stressful life events increase vulnerability to problematic alcohol use, and they may do this by disrupting reward-related neural circuitry. This is particularly relevant for adolescents because alcohol use rises sharply after mid-adolescence and alcohol abuse peaks at age 20. Adolescents also report more stressors compared with children, and neural reward circuitry may be especially vulnerable to stressors during adolescence because of prefrontal cortex remodeling. Using a large sample of male participants in a longitudinal functional magnetic resonance imaging study (N = 157), we evaluated whether cumulative stressful life events between the ages of 15 and 18 were associated with reward-related brain function and problematic alcohol use at age 20 years. Higher cumulative stressful life events during adolescence were associated with decreased response in the medial prefrontal cortex (mPFC) during monetary reward anticipation and following the receipt of monetary rewards. Stress-related decreases in mPFC response during reward anticipation and following rewarding outcomes were associated with the severity of alcohol dependence. Furthermore, mPFC response mediated the association between stressful life events and later symptoms of alcohol dependence. These data are consistent with neurobiological models of addiction that propose that stressors during adolescence increase risk for problematic alcohol use by disrupting reward circuit function.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24795442</PMID><DateCreated><Year>2015</Year><Month>03</Month><Day>06</Day></DateCreated><DateCompleted><Year>2016</Year><Month>05</Month><Day>12</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1749-5024</ISSN><JournalIssue CitedMedium="Internet"><Volume>10</Volume><Issue>3</Issue><PubDate><Year>2015</Year><Month>Mar</Month></PubDate></JournalIssue><Title>Social cognitive and affective neuroscience</Title><ISOAbbreviation>Soc Cogn Affect Neurosci</ISOAbbreviation></Journal><ArticleTitle>Life stress in adolescence predicts early adult reward-related brain function and alcohol dependence.</ArticleTitle><Pagination><MedlinePgn>416-23</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1093/scan/nsu061</ELocationID><Abstract><AbstractText>Stressful life events increase vulnerability to problematic alcohol use, and they may do this by disrupting reward-related neural circuitry. This is particularly relevant for adolescents because alcohol use rises sharply after mid-adolescence and alcohol abuse peaks at age 20. Adolescents also report more stressors compared with children, and neural reward circuitry may be especially vulnerable to stressors during adolescence because of prefrontal cortex remodeling. Using a large sample of male participants in a longitudinal functional magnetic resonance imaging study (N = 157), we evaluated whether cumulative stressful life events between the ages of 15 and 18 were associated with reward-related brain function and problematic alcohol use at age 20 years. Higher cumulative stressful life events during adolescence were associated with decreased response in the medial prefrontal cortex (mPFC) during monetary reward anticipation and following the receipt of monetary rewards. Stress-related decreases in mPFC response during reward anticipation and following rewarding outcomes were associated with the severity of alcohol dependence. Furthermore, mPFC response mediated the association between stressful life events and later symptoms of alcohol dependence. These data are consistent with neurobiological models of addiction that propose that stressors during adolescence increase risk for problematic alcohol use by disrupting reward circuit function.</AbstractText><CopyrightInformation>© The Author (2014). Published by Oxford University Press. For Permissions, please email: journals.permissions@oup.com.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Casement</LastName><ForeName>Melynda D</ForeName><Initials>MD</Initials><AffiliationInfo><Affiliation>Department of Psychiatry, Department of Psychology, Department of Pediatrics, and Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, PA, USA 15213 Department of Psychiatry, Department of Psychology, Department of Pediatrics, and Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, PA, USA 15213 forbese@upmc.edu.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shaw</LastName><ForeName>Daniel S</ForeName><Initials>DS</Initials><AffiliationInfo><Affiliation>Department of Psychiatry, Department of Psychology, Department of Pediatrics, and Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, PA, USA 15213.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sitnick</LastName><ForeName>Stephanie L</ForeName><Initials>SL</Initials><AffiliationInfo><Affiliation>Department of Psychiatry, Department of Psychology, Department of Pediatrics, and Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, PA, USA 15213.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Musselman</LastName><ForeName>Samuel C</ForeName><Initials>SC</Initials><AffiliationInfo><Affiliation>Department of Psychiatry, Department of Psychology, Department of Pediatrics, and Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, PA, USA 15213.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Forbes</LastName><ForeName>Erika E</ForeName><Initials>EE</Initials><AffiliationInfo><Affiliation>Department of Psychiatry, Department of Psychology, Department of Pediatrics, and Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, PA, USA 15213 Department of Psychiatry, Department of Psychology, Department of Pediatrics, and Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, PA, USA 15213 Department of Psychiatry, Department of Psychology, Department of Pediatrics, and Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, PA, USA 15213 Department of Psychiatry, Department of Psychology, Department of Pediatrics, and Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, PA, USA 15213.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>DA026222</GrantID><Acronym>DA</Acronym><Agency>NIDA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 MH050907</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 DA026222</GrantID><Acronym>DA</Acronym><Agency>NIDA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01-MH050907</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01-MH093605</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 MH093605</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>05</Month><Day>01</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Soc Cogn Affect 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