Bader Chaarani1, Kees-Jan Kan2, Scott Mackey2, Philip A Spechler2, Alexandra Potter2, Catherine Orr2, Nicholas D'Alberto2, Kelsey E Hudson2, Tobias Banaschewski3, Arun L W Bokde4, Uli Bromberg5, Christian Büchel5, Anna Cattrell6, Patricia J Conrod7, Sylvane Desrivières6, Herta Flor8, Vincent Frouin9, Jürgen Gallinat10, Penny Gowland11, Andreas Heinz12, Bernd Ittermann13, Jean-Luc Martinot14, Frauke Nees15, Dimitri Papadopoulos-Orfanos9, Tomáš Paus16, Luise Poustka17, Michael N Smolka18, Henrik Walter12, Robert Whelan19, Stephen T Higgins2, Gunter Schumann20, Robert R Althoff2, Elliot A Stein21, Hugh Garavan22. 1. Vermont Center on Behavior and Health, Departments of Psychiatry and Psychology, University of Vermont, Burlington, Vermont. Electronic address: melmarsr@uvm.edu. 2. Vermont Center on Behavior and Health, Departments of Psychiatry and Psychology, University of Vermont, Burlington, Vermont. 3. Department of Child and Adolescent Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany. 4. Discipline of Psychiatry, School of Medicine and Trinity College Institute of Neurosciences, Trinity College Dublin, Dublin, Ireland. 5. University Medical Centre Hamburg-Eppendorf, Hamburg, Germany. 6. Medical Research Council-Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King's College London, United Kingdom. 7. Department of Psychological Medicine and Psychiatry, Institute of Psychiatry, Psychology and Neuroscience, King's College London, United Kingdom; Department of Psychiatry, Université de Montreal, CHU Ste Justine Hospital, Montreal, Quebec. 8. Department of Cognitive and Clinical Neuroscience, Central Institute of Mental Health, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany; Department of Psychology, School of Social Sciences, University of Mannheim, Mannheim, Germany. 9. Neurospin, Commissariat à l'Energie Atomique, CEA-Saclay Center, Paris, France. 10. Department of Psychiatry and Psychotherapy, Hamburg, Germany. 11. Sir Peter Mansfield Imaging Centre, School of Physics and Astronomy, University of Nottingham, University Park, Nottingham, United Kingdom. 12. Department of Psychiatry and Psychotherapy, Campus Charité Mitte, Charité, Universitätsmedizin Berlin, Berlin, Germany. 13. Physikalisch-Technische Bundesanstalt, Braunschweig and Berlin, Germany. 14. Institut National de la Santé et de la Recherche Médicale, INSERM Unit 1000 "Neuroimaging and Psychiatry," University Paris Sud, University Paris Descartes-Sorbonne Paris Cité and Maison de Solenn, Paris, France. 15. Department of Child and Adolescent Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany; Department of Psychology, School of Social Sciences, University of Mannheim, Mannheim, Germany. 16. Rotman Research Institute, Baycrest and Departments of Psychology and Psychiatry, University of Toronto, Toronto, Ontario, Canada. 17. Department of Child and Adolescent Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany; Department of Child and Adolescent Psychiatry and Psychotherapy, Medical University of Vienna, Austria. 18. Department of Psychiatry and Neuroimaging Center, Technische Universität Dresden, Dresden, Germany. 19. Department of Psychology, University College Dublin, Dublin, Ireland. 20. Department of Psychiatry, Université de Montreal, CHU Ste Justine Hospital, Montreal, Quebec. 21. The National Institute on Drug Abuse Intramural Research Program, National Institutes of Health, Baltimore, Maryland. 22. Vermont Center on Behavior and Health, Departments of Psychiatry and Psychology, University of Vermont, Burlington, Vermont. Electronic address: hgaravan@uvm.edu.
Abstract
BACKGROUND: Studying the neural consequences of tobacco smoking during adolescence, including those associated with early light use, may help expose the mechanisms that underlie the transition from initial use to nicotine dependence in adulthood. However, only a few studies in adolescents exist, and they include small samples. In addition, the neural mechanism, if one exists, that links nicotinic receptor genes to smoking behavior in adolescents is still unknown. METHODS: Structural and diffusion tensor magnetic resonance imaging data were acquired from a large sample of 14-year-old adolescents who completed an extensive battery of neuropsychological, clinical, personality, and drug-use assessments. Additional assessments were conducted at 16 years of age. RESULTS: Exposure to smoking in adolescents, even at low doses, is linked to volume changes in the ventromedial prefrontal cortex and to altered neuronal connectivity in the corpus callosum. The longitudinal analyses strongly suggest that these effects are not preexisting conditions in those who progress to smoking. There was a genetic contribution wherein the volume reduction effects were magnified in smokers who were carriers of the high-risk genotype of the alpha 5 nicotinic receptor subunit gene, rs16969968. CONCLUSIONS: These findings give insight into a mechanism involving genes, brain structure, and connectivity underlying why some adolescents find nicotine especially addictive. Published by Elsevier Inc.
BACKGROUND: Studying the neural consequences of tobacco smoking during adolescence, including those associated with early light use, may help expose the mechanisms that underlie the transition from initial use to nicotine dependence in adulthood. However, only a few studies in adolescents exist, and they include small samples. In addition, the neural mechanism, if one exists, that links nicotinic receptor genes to smoking behavior in adolescents is still unknown. METHODS: Structural and diffusion tensor magnetic resonance imaging data were acquired from a large sample of 14-year-old adolescents who completed an extensive battery of neuropsychological, clinical, personality, and drug-use assessments. Additional assessments were conducted at 16 years of age. RESULTS: Exposure to smoking in adolescents, even at low doses, is linked to volume changes in the ventromedial prefrontal cortex and to altered neuronal connectivity in the corpus callosum. The longitudinal analyses strongly suggest that these effects are not preexisting conditions in those who progress to smoking. There was a genetic contribution wherein the volume reduction effects were magnified in smokers who were carriers of the high-risk genotype of the alpha 5 nicotinic receptor subunit gene, rs16969968. CONCLUSIONS: These findings give insight into a mechanism involving genes, brain structure, and connectivity underlying why some adolescents find nicotine especially addictive. Published by Elsevier Inc.
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