Funk D, Marinelli PW, Le AD. Biological processes underlying co-use of alcohol and nicotine: neuronal mechanisms, cross-tolerance, and genetic factors. Alcohol Res Health 29: 186-192

Centre for Addiction and Mental Health, Toronto, Canada.
Alcohol research & health: the journal of the National Institute on Alcohol Abuse and Alcoholism (Impact Factor: 0.58). 02/2006; 29(3):186-92.
Source: PubMed


Alcohol and nicotine are two of the oldest and most commonly used recreational drugs, and many people use both of them together. Although their ready availability likely contributes to the strong correlation between alcohol and nicotine use, several lines of evidence suggest that biological factors play a role as well. For example, both alcohol and nicotine act on a brain system called the mesolimbic dopamine system, which mediates the rewarding and reinforcing properties of both drugs. Modification of the activities of the mesolimbic dopamine system can interfere with the effects of both alcohol and nicotine. Another mechanism that may contribute to alcohol-nicotine interactions is cross-tolerance to the effects of both drugs. Finally, genetic studies in humans and of selectively bred mouse and rat strains suggest that shared genetic factors help determine a person's liability to use or abuse both alcohol and nicotine.

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    • "It is thus possible that the minor allele of the rs2948694 alters the sensitivity of the cholinergic-dopaminergic reward link, which in turn may lead to a predisposition to smoking and increased alcohol consumption, reflected by the higher AUDIT scores in the present study. Previous studies show that alcohol and nicotine dependence share a genetic background (True et al. 1999; Funk, Marinelli & Le 2006; von der Pahlen et al. 2008). This is further supported by the welldocumented co-use of alcohol and nicotine—also observed in the present study—and the neurobiological interaction between alcohol and nicotine within the mesolimbic dopamine system (for review, see Larsson & Engel 2004; Soderpalm, Lof & Ericson 2009). "
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    • "For example, pharmacological and/or genetic manipulation of various nAChRs such as α4β2*, α3β4*, and α3/α6β2* subtypes (* indicates the possible inclusion of other subunits) were shown to modulate ethanol selfadministration and ethanol-induced elevation of accumbal dopamine levels in rodents (Chatterjee et al., 2011; Hendrickson et al., 2010; Jerlhag et al., 2006; Kamens et al., 2010). Moreover, given the strong correlation between nicotine and ethanol abuse (DiFranza and Guerrera, 1990; Funk et al., 2006), it was further demonstrated that nicotine treatment re-instates ethanol seeking behaviors in rats following extinction of ethanol reinforcement (Lê et al., 2003; Hauser et al., 2012). In addition, nAChRs are previously shown to regulate deprivation-induced re-exposure of ethanol seeking in long-term ethanol experienced rats (Kuzmin et al., 2009; Rezvani et al., 2010). "
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    • "In addition to psychosocial and genetic factors (Bobo and Husten, 2000; Schlaepfer et al., 2008), evidence suggests that the interactions between nicotine and alcohol arise from shared pharmacological actions (Funk et al., 2006; Hurley et al., 2012; Larsson and Engel, 2004). These drugs activate common neural substrates, including the mesolimbic dopamine (DA) system (De Biasi and Dani, 2011; Di Chiara, 2000; Gonzales et al., 2004) and the hypothalamic-pituitary-adrenal (HPA) axis associated with stress hormone signaling (Armario, 2010; Lutfy et al., 2012; Richardson et al., 2008). "
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