Tobacco Use is Associated With Reduced Central Serotonergic Neurotransmission in Type 1 Alcohol-Dependent Individuals

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Abstract
Reduced central serotonergic neurotransmission in alcohol dependence may be attributed to the effects of cigarette smoking (and possibly more specifically to nicotine) rather than to alcoholism or its subtypes. The aim of the present study was therefore to compare central serotonergic neurotransmission in tobacco-using (cigarette smokers and users of smokeless tobacco, i.e., snuffers) alcohol-dependent individuals to that of tobacco-nonusing alcohol-dependent individuals. The central serotonergic neurotransmission was assessed by the prolactin (PRL) response to the serotonin-releasing agent D-fenfluramine (30 mg orally). Male subjects (n = 37) aged 20-65 years were recruited for this purpose. They were all type 1 alcohol-dependent individuals and had ended their alcohol intake the day before the D-fenfluramine challenge test. There was no difference in baseline PRL concentrations between tobacco-using (n = 18) and tobacco-nonusing (n = 19) alcohol-dependent individuals. On the other hand, the maximum PRL response after D-fenfluramine was significantly lower in the tobacco-using group as compared to the tobacco-nonusing individuals. Whether the reduction in central serotonergic neurotransmission in tobacco-using alcohol-dependent individuals is pre-existing or a result of tobacco use remains to be elucidated.