A hallmark of drug addiction, including tobacco smoking addiction, is a dysfunctional
dopaminergic reward system. Positron emission tomography (PET) neuroimaging has been
used to identify persistent deficits in the availability of striatal dopamine D2/D3 receptors across various addictions, including alcohol, cocaine, heroin, amphetamine,
and nicotine (
1
). These findings suggest that addiction leads to a chronic downregulation in the
number of dopamine D2/D3 receptors. In addition, a “blunted” dopamine response to an amphetamine challenge
has been documented in both alcohol-dependent (
2
) and cocaine-dependent (
3
) individuals several weeks after the last drug use compared to healthy controls;
the more blunted the response, the worse the treatment outcome (
3
). This suggests that individuals with dysfunctional dopamine transmission are not
able to effectively transition from drug-reinforced behavior to more natural alternative
rewards. Lower levels of other markers of dopamine neurotransmission, including striatal
D1 receptors (
4
), have also been noted in tobacco smokers versus nonsmokers. A functional, responsive
reward system is critical for long-term abstinence; however, within-subject longitudinal
studies that examine changes in neurochemistry during recovery from addiction are
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References
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Article info
Publication history
Accepted:
May 25,
2016
Received:
May 23,
2016
Identification
Copyright
© 2016 Society of Biological Psychiatry.
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- Effects of Smoking Cessation on Presynaptic Dopamine Function of Addicted Male SmokersBiological PsychiatryVol. 80Issue 3
- PreviewThere 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.
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