Summary: Researchers report smoking related deficits in dopamine return to normal three months after quitting.
A new study in Biological Psychiatry reports that smoking-related deficits in brain dopamine, a chemical implicated in reward and addiction, return to normal three months after quitting. The normalization of dopamine systems suggests smoking-related deficits are a consequence of chronic smoking, rather than a risk factor. These findings raise the possibility that treatments might be developed that normalize the dopamine system in smokers.
According to first author Dr. Lena Rademacher, postdoctoral fellow at the University of Lübeck in Germany, a major challenge in understanding substance-related disorders lies in uncovering why only some individuals become addicted.
Researchers think some people could possess a trait that predisposes them to addiction, and suspect that brain circuits involving dopamine may be involved. Drugs of abuse release dopamine, and addiction to nicotine is associated with abnormalities in the dopamine system. But researchers are uncertain if smoking induces those abnormalities or if they already exist and contribute to risk of nicotine addiction.
Senior author Dr. Ingo Vernaleken, Professor at RWTH Aachen University in Germany, led a team of researchers examining dopamine function in chronic smokers before and after long-term cessation. The researchers used a brain imaging technique called positron emission tomography to measure an index of the capacity for dopamine production in 30 men who were nicotine-dependent smokers and 15 nonsmokers. After performing an initial scan on all participants, 15 smokers who successfully quit were scanned again after three months of abstinence from smoking and nicotine replacement.
The initial scan revealed a 15-20% reduction in the capacity for dopamine production in smokers compared with nonsmokers. The researchers expected this impairment to persist even after quitting, which would suggest it could be a marker of vulnerability for nicotine addiction. “Surprisingly, the alterations in dopamine synthesis capacity normalized through abstinence,” said Rademacher.
The role of dopamine in vulnerability toward nicotine addiction cannot be excluded, but the findings suggest that altered dopamine function of smokers is a consequence of nicotine consumption rather than the cause.
Dr. John Krystal, Editor of Biological Psychiatry, noted the implications of these findings for developing better ways to help smokers trying to quit. “This study suggests that the first three months after one stops smoking may be a particularly vulnerable time for relapse, in part, because of persisting dopamine deficits. This observation raises the possibility that one might target these deficits with new treatments.”
About this neuroscience research article
Source: Rhiannon Bugno – Elsevier Image Source: This NeuroscienceNews.com image is in the public domain. Original Research:Abstract for “Effects of Smoking Cessation on Presynaptic Dopamine Function of Addicted Male Smokers” by Lena Rademacher, Susanne Prinz, Oliver Winz, Karsten Henkel, Claudia A. Dietrich, Jörn Schmaljohann, Siamak Mohammadkhani Shali, Ina Schabram, Christian Stoppe, Paul Cumming, Ralf-Dieter Hilgers, Yoshitaka Kumakura, Mark Coburn, Felix M. Mottaghy, Gerhard Gründer, and Ingo Vernaleken in Biological Psychiatry. Published online July 28 2016 doi:10.1016/j.biopsych.2015.11.009
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[cbtabs][cbtab title=”MLA”]Elsevier. “Recovery of Dopamine Function Emerges With Recovery From Smoking.” NeuroscienceNews. NeuroscienceNews, 28 July 2016. <https://neurosciencenews.com/dopamine-smoking-neuroscience-4751/>.[/cbtab][cbtab title=”APA”]Elsevier. (2016, July 28). Recovery of Dopamine Function Emerges With Recovery From Smoking. NeuroscienceNew. Retrieved July 28, 2016 from https://neurosciencenews.com/dopamine-smoking-neuroscience-4751/[/cbtab][cbtab title=”Chicago”]Elsevier. “Recovery of Dopamine Function Emerges With Recovery From Smoking.” https://neurosciencenews.com/dopamine-smoking-neuroscience-4751/ (accessed July 28, 2016).[/cbtab][/cbtabs]
Effects of Smoking Cessation on Presynaptic Dopamine Function of Addicted Male Smokers
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-[18F]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.
“Effects of Smoking Cessation on Presynaptic Dopamine Function of Addicted Male Smokers” by Lena Rademacher, Susanne Prinz, Oliver Winz, Karsten Henkel, Claudia A. Dietrich, Jörn Schmaljohann, Siamak Mohammadkhani Shali, Ina Schabram, Christian Stoppe, Paul Cumming, Ralf-Dieter Hilgers, Yoshitaka Kumakura, Mark Coburn, Felix M. Mottaghy, Gerhard Gründer, and Ingo Vernaleken in Biological Psychiatry. Published online July 28 2016 doi:10.1016/j.biopsych.2015.11.009