Lena Rademacher1, Susanne Prinz2, Oliver Winz3, Karsten Henkel4, Claudia A Dietrich4, Jörn Schmaljohann3, Siamak Mohammadkhani Shali3, Ina Schabram4, Christian Stoppe5, Paul Cumming6, Ralf-Dieter Hilgers7, Yoshitaka Kumakura8, Mark Coburn9, Felix M Mottaghy10, Gerhard Gründer11, Ingo Vernaleken11. 1. Department of Psychiatry, Psychotherapy and Psychosomatics, RWTH Aachen University, Aachen; Department of Psychiatry and Psychotherapy, Social Neuroscience Laboratory, University of Lübeck, Lübeck, Germany. Electronic address: Rademacher@snl.uni-luebeck.de. 2. Department of Psychiatry, Psychotherapy and Psychosomatics, RWTH Aachen University, Aachen; Department of Psychiatry and Psychotherapy, Centre for Integrative Psychiatry, University of Zürich, Rheinau, Switzerland. 3. Department of Nuclear Medicine, RWTH Aachen University, Aachen. 4. Department of Psychiatry, Psychotherapy and Psychosomatics, RWTH Aachen University, Aachen. 5. Department of Anesthesiology, RWTH Aachen University, Aachen; Institute of Biochemistry and Molecular Cell Biology, RWTH Aachen University, Aachen. 6. Department of Neuropsychiatry and Psychosomatic Medicine, Oslo University Hospital, Oslo, Norway; School of Psychology and Counselling, Queensland University of Technology, Brisbane, Queensland, Australia. 7. Department of Medical Statistics, RWTH Aachen University, Aachen. 8. Department of Pharmacology and Neuroscience, University of Copenhagen, Copenhagen, Denmark. 9. Department of Anesthesiology, RWTH Aachen University, Aachen. 10. Department of Nuclear Medicine, RWTH Aachen University, Aachen; Jülich/Aachen Research Alliance, Aachen, Germany; Department of Nuclear Medicine, Maastricht University Medical Center, Maastricht, The Netherlands. 11. Department of Psychiatry, Psychotherapy and Psychosomatics, RWTH Aachen University, Aachen; Jülich/Aachen Research Alliance, Aachen, Germany.
Abstract
BACKGROUND: There is evidence of abnormal cerebral dopamine transmission in nicotine-dependent smokers, but it is unclear whether dopaminergic abnormalities are due to acute nicotine abuse or whether they persist with abstinence. We addressed this question by conducting longitudinal positron emission tomography (PET) examination of smokers before and after 3 months of abstinence. METHODS: We obtained baseline 6-[(18)F]fluoro-L-DOPA (FDOPA)-PET scans in 15 nonsmokers and 30 nicotine-dependent smokers, who either smoked as per their usual habit or were in acute withdrawal. All smokers then underwent cessation treatment, and successful abstainers were re-examined by FDOPA-PET after 3 months of abstinence (n = 15). Uptake of FDOPA was analyzed using a steady-state model yielding estimates of the dopamine synthesis capacity (K); the turnover of tracer dopamine formed in living brain (kloss); and the tracer distribution volume (Vd), which is an index of dopamine storage capacity. RESULTS: Compared with nonsmokers, K was 15% to 20% lower in the caudate nuclei of consuming smokers. Intraindividual comparisons of consumption and long-term abstinence revealed significant increases in K in the right dorsal and left ventral caudate nuclei. Relative to acute withdrawal, Vd significantly decreased in the right ventral and dorsal caudate after prolonged abstinence. Severity of nicotine dependence significantly correlated with dopamine synthesis capacity and dopamine turnover in the bilateral ventral putamen of consuming smokers. CONCLUSIONS: The results suggest a lower dopamine synthesis capacity in nicotine-dependent smokers that appears to normalize with abstinence. Further investigations are needed to clarify the role of dopamine in nicotine addiction to help develop smoking prevention and cessation treatments.
BACKGROUND: There is evidence of abnormal cerebral dopamine transmission in nicotine-dependent smokers, but it is unclear whether dopaminergic abnormalities are due to acute nicotine abuse or whether they persist with abstinence. We addressed this question by conducting longitudinal positron emission tomography (PET) examination of smokers before and after 3 months of abstinence. METHODS: We obtained baseline 6-[(18)F]fluoro-L-DOPA (FDOPA)-PET scans in 15 nonsmokers and 30 nicotine-dependent smokers, who either smoked as per their usual habit or were in acute withdrawal. All smokers then underwent cessation treatment, and successful abstainers were re-examined by FDOPA-PET after 3 months of abstinence (n = 15). Uptake of FDOPA was analyzed using a steady-state model yielding estimates of the dopamine synthesis capacity (K); the turnover of tracer dopamine formed in living brain (kloss); and the tracer distribution volume (Vd), which is an index of dopamine storage capacity. RESULTS: Compared with nonsmokers, K was 15% to 20% lower in the caudate nuclei of consuming smokers. Intraindividual comparisons of consumption and long-term abstinence revealed significant increases in K in the right dorsal and left ventral caudate nuclei. Relative to acute withdrawal, Vd significantly decreased in the right ventral and dorsal caudate after prolonged abstinence. Severity of nicotine dependence significantly correlated with dopamine synthesis capacity and dopamine turnover in the bilateral ventral putamen of consuming smokers. CONCLUSIONS: The results suggest a lower dopamine synthesis capacity in nicotine-dependent smokers that appears to normalize with abstinence. Further investigations are needed to clarify the role of dopamine in nicotine addiction to help develop smoking prevention and cessation treatments.
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