2011
DOI: 10.1111/j.1369-1600.2010.00309.x
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Abstract: Alcohol and nicotine use disorders are often treated as separate diseases, despite evidence that approximately 80-90% of alcohol dependent individuals are also heavy smokers. Both nicotine and ethanol have been shown to interact with neuronal nicotinic acetylcholine receptors (nAChRs), suggesting these receptors are a common biological target for the effects of nicotine and ethanol in the brain. There are few studies that have examined the effects of co-administered nicotine and ethanol on the activity of nACh… Show more

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Cited by 97 publications
(99 citation statements)
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References 57 publications
(78 reference statements)
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“…During IV self-administration of nicotine and ethanol together, BEC levels were significantly higher ( p < 0.01) in the fat-stimulated (120 ± 10.2 mg/dL) compared to chow (85 ± 9.3 mg/dL) offspring. These BEC levels in the chow group, which exceed those commonly achieved in Sprague Dawley rats (Barson, Fagan, Chang, & Leibowitz, 2013; Bito-Onon et al, 2011), are comparable to those found in selectively bred alcohol-preferring P rats (Bell, Rodd, Lumeng, Murphy, & McBride, 2006). Furthermore, BEC levels in the fat-exposed rats are equivalent to those found after an alcohol binge or during alcohol relapse in the P rats (Bell et al, 2006; Rodd-Henricks et al, 2001).…”
Section: Discussionsupporting
confidence: 67%
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“…During IV self-administration of nicotine and ethanol together, BEC levels were significantly higher ( p < 0.01) in the fat-stimulated (120 ± 10.2 mg/dL) compared to chow (85 ± 9.3 mg/dL) offspring. These BEC levels in the chow group, which exceed those commonly achieved in Sprague Dawley rats (Barson, Fagan, Chang, & Leibowitz, 2013; Bito-Onon et al, 2011), are comparable to those found in selectively bred alcohol-preferring P rats (Bell, Rodd, Lumeng, Murphy, & McBride, 2006). Furthermore, BEC levels in the fat-exposed rats are equivalent to those found after an alcohol binge or during alcohol relapse in the P rats (Bell et al, 2006; Rodd-Henricks et al, 2001).…”
Section: Discussionsupporting
confidence: 67%
“…Also, a specific paradigm involving sequential administration of the two drugs may yield results reflecting the effect of one drug on intake of the other, rather than the co-use of these drugs. This is suggested by studies showing that the injection of nicotine can stimulate the drinking of ethanol and that rats prone to drinking excess ethanol are subsequently found to self-administer more nicotine (Bito-Onon et al, 2011; Lê et al, 2000, 2003, 2006; Olausson et al, 2001). Our model, which involves the IV method of self-administration of both drugs and their simultaneous administration, eliminates both of these possible confounding factors while showing greater self-administration of the nicotine/ethanol mixture as compared to nicotine or ethanol alone.…”
Section: Discussionmentioning
confidence: 99%
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“…Thus, the population of ENK neurons stimulated in these areas, perhaps acting in conjunction with circulating lipids, may direct appetitive actions that increase the chances of these three substances being consumed again, and they may also increase chow intake, although this remains to be tested using the current dosing paradigm. This evidence, showing increased activation of ENK-expressing neurons in specific nuclei with a high degree of interconnectivity, suggests that the positive relationship which exists between ENK and these reinforcing substances is a defining commonality that allows the intake of one of these three substances to stimulate intake of the others (Carrillo et al, 2004; Barson et al, 2009; Bito-Onon et al, 2011), ultimately leading to overconsumption and potential abuse of any or all of the substances.…”
Section: 5 Conclusionmentioning
confidence: 93%
“…For example, rodents exposed to nicotine increase alcohol self-administration (Le et al, 2003; Lopez-Moreno et al, 2004), whereas systemic or central administration of nicotine receptor partial agonist or antagonist reduces alcohol consumption and/or preference (Bito-Onon et al, 2011; Steensland et al, 2007; Blomqvist et al, 1996). Although nicotine is believed to be one of the greatest risk factor for the development of alcoholism, little is known about underlying neurobiological mechanisms responsible for nicotine and alcohol co-abuse (Davis and de Fiebre, 2006).…”
Section: Introductionmentioning
confidence: 99%