Nicotinic mechanisms involved in the dopamine activating and reinforcing properties of ethanol

Söderpalm, Bo; Ericson, Mia; Olausson, Peter; Blomqvist, Ola; Engel, Jörgen A.

doi:10.1016/s0166-4328(00)00203-5

Cited by 211 publications

(148 citation statements)

References 71 publications

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“…In humans, high correlations have been found between alcohol and nicotine use: the prevalence of smoking in alcoholics is approximately three times higher than in the general population (Istvan and Matarazzo, 1984;Kandel et al, 1997). Results from studies using laboratory rats are in agreement with these correlational data in humans (Soderpalm et al, 2000). For example, repeated treatment with nicotine increases home-cage intake and operant self-administration of alcohol (Lê et al, 2000;Olausson et al, 2001), and nicotine injections reinstate alcohol seeking in a rat model of relapse to drugs (Lê et al, 2003); however, although nicotine can potentiate alcohol-taking behavior, no studies have been published regarding the effect of alcohol exposure on nicotine-taking behavior.…”

Section: Introductionsupporting

confidence: 67%

Increased Vulnerability to Nicotine Self-Administration and Relapse in Alcohol-Naive Offspring of Rats Selectively Bred for High Alcohol Intake

et al. 2006

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The prevalence of smoking in human alcoholics is substantially higher than in the general population, and results from twin studies suggest that a shared genetic vulnerability underlies alcohol and nicotine addiction. Here, we directly tested this hypothesis by examining nicotine-taking behavior in alcohol-naive offspring of alcohol-preferring (P) rats and alcohol-nonpreferring (NP) rats that had been selectively bred for high and low alcohol intake. The self-administration of intravenous nicotine (0.015-0.060 mg/kg per infusion) in P rats was more than twice than that of NP rats. Nicotine seeking induced by reexposure to nicotine cues in extinction tests was also substantially greater in P rats than in NP rats. In a subsequent relapse test, priming nicotine injections reinstated drug seeking in P rats but not NP rats. P rats also self-administered higher amounts of oral sucrose (1-20%) than NP rats, a finding consistent with previous reports. In contrast, self-administration of intravenous cocaine (0.1875-1.125 mg/kg per infusion) was remarkably similar in the P and NP rats; however, P-NP differences in cocaine seeking emerged in subsequent extinction and cocaine priming-induced reinstatement tests. In both cases, lever responding was higher in P rats than in NP rats. Thus, alcohol-naive offspring of rats genetically selected for high alcohol intake are highly susceptible to nicotine self-administration and relapse, and this susceptibility is not likely caused by general reward deficits in NP rats. The present findings provide experimental evidence for the hypothesis that a shared genetic determinant accounts for the co-abuse of nicotine and alcohol.

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Section: Introductionsupporting

confidence: 67%

Increased Vulnerability to Nicotine Self-Administration and Relapse in Alcohol-Naive Offspring of Rats Selectively Bred for High Alcohol Intake

et al. 2006

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“…Accordingly, the nicotinic receptor is a site at which nicotine and ethanol may interact. Corroborating this suggestion, it has been demonstrated that ethanol enhances agonist-induced ion flux through nicotinic receptors (Aistrup et al, 1999;Cardoso et al, 1999) and that ethanol-induced stimulation of mesolimbic dopamine systems involves the activation of nicotinic receptors (Soderpalm et al, 2000). Despite these findings, there have been relatively few animal studies of the basic neurobiology of the combined nicotine and ethanol exposure, and while some studies suggest that nicotine has a modulatory effect on ethanol effects through its cholinergic actions, others show no marked interactions and still others show augmented effects (Bachtell and Ryabinin, 2001;Penland et al, 2001;Tizabi et al, 2002Tizabi et al, , 2003.…”

Section: Neurobiology Of Nicotine Vs Ethanol Interactionsmentioning

confidence: 94%

Combined Exposure to Nicotine and Ethanol in Adolescent Mice Differentially Affects Anxiety Levels during Exposure, Short-Term, and Long-Term Withdrawal

Abreu‐Villaça

Nunes

Queiroz-Gomes

et al. 2007

Neuropsychopharmacol

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Smoking and consumption of alcoholic beverages are frequently associated during adolescence. This association could be explained by the cumulative behavioral effects of nicotine and ethanol, particularly those related to anxiety levels. However, despite epidemiological findings, there have been few animal studies of the basic neurobiology of the combined exposure in the adolescent brain. In the present work we assessed, through the use of the elevated plus maze, the short-and long-term anxiety effects of nicotine (NIC) and/or ethanol (ETOH) exposure during adolescence (from the 30th to the 45th postnatal day) in four groups of male and female C57BL/6 mice: (1) Concomitant NIC (nicotine free-base solution (50 mg/ml) in 2% saccharin to drink) and ETOH (ethanol solution (25%, 2 g/kg) i.p. injected every other day) exposure; (2) NIC exposure; (3) ETOH exposure; (4) Vehicle. C57BL/6 mice were selected, in spite of the fact that they present slower ethanol metabolism, because they readily consume nicotine in the concentration used in the present study. During exposure (45th postnatal day: PN45), our results indicated that ethanol was anxiolytic in adolescent mice and that nicotine reverted this effect. Short-term drug withdrawal (PN50) elicited sex-dependent effects: exposure to nicotine and/or ethanol was anxiogenic only for females. Although neither nicotine nor ethanol effects persisted up to 1 month postexposure (PN75), the coadministration elicited an anxiogenic response. In spite of the fact that generalizations based on the results from a single strain of mice are prone to shortcomings, our results suggest that the deficient response to the anxiolytic effects of ethanol in adolescents co-exposed to nicotine may drive higher ethanol consumption. Additionally, increased anxiety during long-term smoking and drinking withdrawal may facilitate relapse to drug use.

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“…Addictive substances, including nicotine and alcohol, are believed to exert their rewarding effects by stimulating release of nucleus accumbens DA and opioid peptides (Gianoulakis, 2004;Soderpalm, et al, 2000). Relatedly, chronic substance use is associated with hypoactivity in the mesolimbic DA pathway (Altmann et al, 1996;Volkow et al, 2004) and the opioid system (Drews and Zimmer, 2010).…”

mentioning

confidence: 99%

Effects of nicotine and alcohol on affective responses to emotionally toned film clips

Dawkins

Powell

2011

Psychopharmacology

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2Rationale: Smoking abstinence can result in decreased affective reactions to positively valenced stimuli and this can be reversed via smoking. Given their shared ability to trigger nucleus accumbens dopamine release, a priming dose of alcohol may likewise augment positive affective responses during abstinence. AbstractObjectives: To replicate our previous finding that compared to satiation, abstinence from smoking will be associated with decreased 'happiness' responses to positively valenced film clips (study 1); and to explore whether a priming dose of alcohol can substitute for nicotine by concomitantly enhancing such responses (study 2). In both studies 'sadness' responses to negatively valenced clips were also included.Methods: 32 and 77 smokers respectively in studies 1 and 2 were randomly allocated to abstain from smoking for 10 hours (abstinent smokers) or smoke as usual (satiated smokers).Participants then rated the extent to which they felt a list of emotions in response to each of 16 film clips. In study 2, participants were additionally allocated to an alcohol manipulation in which they received either alcohol or placebo.Results: In Study 1, nicotine administration increased abstinent smokers' ratings of happiness and sadness to the corresponding film clips. In Study 2, nicotine and alcohol both enhanced positive reactivity to happy clips, and their effects were not additive. Alcohol but not nicotine likewise enhanced sadness responses to sad clips. Conclusions:Abstinence from smoking can result in blunting of affective responses to positively toned stimuli, an effect that can be ameliorated by both nicotine and alcohol. The impact of nicotine on negative reactivity appears to be less robust.3

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Nicotinic mechanisms involved in the dopamine activating and reinforcing properties of ethanol

Cited by 211 publications

References 71 publications

Increased Vulnerability to Nicotine Self-Administration and Relapse in Alcohol-Naive Offspring of Rats Selectively Bred for High Alcohol Intake

Increased Vulnerability to Nicotine Self-Administration and Relapse in Alcohol-Naive Offspring of Rats Selectively Bred for High Alcohol Intake

Combined Exposure to Nicotine and Ethanol in Adolescent Mice Differentially Affects Anxiety Levels during Exposure, Short-Term, and Long-Term Withdrawal

Effects of nicotine and alcohol on affective responses to emotionally toned film clips

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