Molecular, Neuronal, and Behavioral Effects of Ethanol and Nicotine Interactions

Abstract

Ethanol and nicotine can modulate the activity of several neurotransmitter systems and signalling pathways. Interactions between ethanol and nicotine can also occur via common molecular targets including nicotinic acetylcholine receptors (nAChRs). These effects can induce molecular and synaptic adaptations that over time, are consolidated in brain circuits that reinforce drug-seeking behavior, contribute to the development of withdrawal symptoms during abstinence and increase the susceptibility to relapse. This chapter will discuss the acute and chronic effects of ethanol and nicotine within the mesolimbic reward pathway and brain circuits involved in learning, memory, and withdrawal. Individual and common molecular targets of ethanol and nicotine within these circuits are also discussed. Finally, we review studies that have identified potential molecular and neuronal processes underlying the high incidence of ethanol and nicotine co-use that may contribute to the development of ethanol and nicotine co-addiction.

Profound alteration in reward processing due to a human polymorphism in CHRNA5: a role in alcohol dependence and feeding behavior

“…Since possible direct interactions between EtOH and nACHRs have been reported [29,30], we verified in drug-naïve animals that the EtOH addiction-like phenotypes observed in α5SNP rats were not due to differences in EtOH metabolism. Blood EtOH concentrations were similar between groups at all time-points following a 2 g/kg EtOH injection (Fig.…”

“…Both alcohol and nicotine can modulate signalling pathways implicated in addiction through both distinct and common molecular targets. In fact, EtOH has been shown to act as an allosteric modulator of nAChRs and suggested to alter the balance between activation and desensitization of nAChRs caused by nicotine [30]. Previous studies reported no alterations in EtOH intake in α5 knock-out (KO) mice in a drinkingin-the-dark paradigm [38,40], although EtOH intake was actually decreased in these mice, in a similar paradigm, after a restraint stress [38].…”

“…Alcoholics are three times more likely to smoke than the general population [3], and at higher risk to die from smokingrelated illnesses than from alcohol-related causes [35]. Several mechanisms have been proposed to underlie alcohol and tobacco addiction comorbidity, including cross-cue conditioning, cross-tolerance and -reinforcement [36,37] and nicotinic modulation of alcohol effects [30,38,39]. Both alcohol and nicotine can modulate signalling pathways implicated in addiction through both distinct and common molecular targets.…”

Smokeless tobacco use: its prevalence and relationships with dental symptoms, nutritional status and blood pressure among rural women in Burkina Faso

“…SLT and alcohol are both psychoactive substances containing nicotine and ethanol molecules, respectively [27], and their synergistic interactive effects potentiate physical and psychological pleasure [28]. Therefore, polyconsumption of both tobacco and alcohol was not surprising [29].…”

Smokeless tobacco use: its prevalence and relationships with dental symptoms, nutritional status and blood pressure among rural women in Burkina Faso

“…SLT and alcohol are both psychoactive substances containing nicotine and ethanol molecules, respectively [27] and their synergistic interactive effects potentiate physical and psychological pleasure [28]. That explains why polyconsumption consisting in combining tobacco and alcohol was not surprising [29].…”