Vera Campbell, Ph.D.
Co-Principal Investigator, Department
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.
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.
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.
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