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Alcohol, Nicotine & the Endogenous Opioid System

Yousef Tizabi, Ph.D.
Principal Investigator, Department of Pharmacology
ytizabi@howard.edu
Vera Campbell, Ph.D.
Co-Principal Investigator, Department of Pharmacology

ABSTRACT

A strong positive association between alcohol (ethanol) consumption and cigarette smoking (nicotine intake) is suggested by epidemiological studies. Alcohol has been implicated as a causal factor in increasing cigarette smoking and is considered a major risk factor for relapse during smoking cessation. Similarly, smoking may be a risk factor for alcoholism. Curiously, the incidence of concomitant drinking and smoking remains high despite the observed exaggerated morbidity due to simultaneous consumption of alcohol and tobacco. Indeed, a synergistic interaction between alcohol and tobacco in inducing various cancers, particularly those of the head, neck and esophagus, or in causing gastric ulcers is evident in heavy drinkers and smokers.

Thus, there is an urgent need to develop medications for stopping concurrent drinking and smoking. Numerous studies have evaluated the effects of ethanol or nicotine individually on various neurotransmitter systems and circuitries. However, very few studies have examined the effects of concurrent alcohol and nicotine on such systems. Antinociceptive or analgesic effects of both alcohol and nicotine have been documented. Antinociceptive effects of these drugs may contribute to their abuse. It is well established that the opioid system is the primary mediator of antinociception. Thus, in this study we will evaluate the role of endogenous opioid peptides in the analgesic effects of alcohol, nicotine and their combination.

The long-term goal of this study is to elucidate the roles of specific opioid peptides in concurrent drinking and smoking. Our preliminary results indicate that combinations of alcohol and nicotine have an additive or synergistic antinociceptive effect. Here, we hypothesize that the antinociceptive effects of alcohol and nicotine are mediated through endogenous opioid release in the spinal cord and the periaqueductal gray (PAG), thus implicating both spinal and supraspinal mechanisms.

Moreover, we will determine which opioid receptor subtypes are involved in the antinociceptive effects of alcohol, nicotine or their combination by using selective antagonists to mu, delta and kappa opioid receptors to block the actions of alcohol and/or nicotine. Spinal and supraspinal analgesic effects will be measured by tail-flick and hot plate assays, respectively. In-vivo microdialysis will be performed in PAG and spinal perfusion in the spinal cord. The release of endogenous opioid peptides will be quantified by RIA and ELISA. The results of these studies will provide further insight into alcohol-nicotine interactions and could suggest novel interventions in concomitant drinking and smoking.

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