Preexposure Effects of Nicotine and Acetaldehyde on Conditioned Taste Aversion Induced by Both Drugs

Kunin, Daniel; Latendresse, Mark W.; Gaskin, Stéphane; Smith, Brian R.; Amit, Zalman

doi:10.1016/s0091-3057(00)00284-7

Cited by 19 publications

(12 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It was utilized in the present set of experiments to determine if there were any preexposure effects at the lowest dose of EtOH that might not have been detected by the one-bottle tests in acquisition. The absence of preexposure effects in the two-bottle preference test are not surprising given this greater sensitivity, i.e., such tests detect any degree of aversions and group differences are often not seen as all subjects display significant aversions (see Batsell and Best, 1993; for such effects in other preexposure CTA preparations, see Kunin et al , 2000, Palmatier and Bevins, 2001). …”

Section: Discussionmentioning

confidence: 99%

Exposure to nicotine during periadolescence or early adulthood alters aversive and physiological effects induced by ethanol

Rinker

Hutchison

Chen

et al. 2011

Pharmacology Biochemistry and Behavior

View full text Add to dashboard Cite

The majority of smokers begin their habit during adolescence, which often precedes experimentation with alcohol. Interestingly, very little preclinical work has been done examining how exposure to nicotine during periadolescence impacts the affective properties of alcohol in adulthood. Understanding how periadolescent nicotine exposure influences the aversive effects of alcohol might help to explain why it becomes more acceptable to this preexposed population. Thus, Experiment 1 exposed male Sprague Dawley rats to either saline or nicotine (0.4 mg/kg, IP) from postnatal day 34 to 43 (periadolescence) and then examined changes in the aversive effects of alcohol (0, 0.56, 1.0 and 1.8 g/kg, IP) in adulthood using the conditioned taste aversion (CTA) design. Changes in blood alcohol concentration (BAC) as well as alcohol-induced hypothermia and locomotor suppression were also assessed. To determine if changes seen were specific to nicotine exposure during periadolescence, the procedures were replicated in adults (Experiment 2). Preexposure to nicotine during periadolescence attenuated the acquisition of the alcohol-induced CTAs (at 1.0 g/kg) and the hypothermic effects of alcohol (1.0 g/kg). Adult nicotine preexposure produced similar attenuation in alcohol's aversive (at 1.8 g/kg) and hypothermic (1.8 g/kg) effects. Neither adolescent nor adult nicotine preexposure altered BACs or alcohol-induced locomotor suppression. These results suggest that nicotine can alter the aversive and physiological effects of alcohol, regardless of the age at which exposure occurs, possibly increasing its overall reinforcing value and making it more likely to be consumed.

show abstract

Section: Discussionmentioning

confidence: 99%

Exposure to nicotine during periadolescence or early adulthood alters aversive and physiological effects induced by ethanol

Rinker

Hutchison

Chen

et al. 2011

Pharmacology Biochemistry and Behavior

View full text Add to dashboard Cite

show abstract

“…Studies examining the behavioral effects of ACD, with regard to EtOH reward, have reported that intra-cranial ventricular (ICV) administration of ACD acted to increase the consumption of and preference for EtOH in rodents (Brown et al, 1979, 1980; Amit and Smith, 1985) while peripheral administration of higher doses of ACD produced a conditioned taste aversion in several rat lines (Brown et al, 1978; Aragon et al, 1986; Kunin et al, 2000; Quintanilla et al, 2002; Escarabajal et al, 2003). Utilizing the UChB rat line (an alcohol preferring rat line), researchers have revealed that peripheral ACD exposure, at lower doses (50–100 mg/kg ACD) than those shown to produce a conditioned taste aversion (>200 mg/kg ACD), acted to significantly increase the consumption of EtOH over the two weeks following ACD administration (Tampier and Quintanilla, 2002).…”

Section: Acd Exhibits Rewarding Propertiesmentioning

confidence: 99%

Elucidating the biological basis for the reinforcing actions of alcohol in the mesolimbic dopamine system: the role of active metabolites of alcohol

Deehan¹,

Hauser²,

Wilden³

et al. 2013

Front. Behav. Neurosci.

View full text Add to dashboard Cite

The development of successful pharmacotherapeutics for the treatment of alcoholism is predicated upon understanding the biological action of alcohol. A limitation of the alcohol research field has been examining the effects of alcohol only and ignoring the multiple biological active metabolites of alcohol. The concept that alcohol is a “pro-drug” is not new. Alcohol is readily metabolized to acetaldehyde within the brain. Acetaldehyde is a highly reactive compound that forms a number of condensation products, including salsolinol and iso-salsolinol (acetaldehyde and dopamine). Recent experiments have established that numerous metabolites of alcohol have direct CNS action, and could, in part or whole, mediate the reinforcing actions of alcohol within the mesolimbic dopamine system. The mesolimbic dopamine system originates in the ventral tegmental area (VTA) and projects to forebrain regions that include the nucleus accumbens (Acb) and the medial prefrontal cortex (mPFC) and is thought to be the neurocircuitry governing the rewarding properties of drugs of abuse. Within this neurocircuitry there is convincing evidence that; (1) biologically active metabolites of alcohol can directly or indirectly increase the activity of VTA dopamine neurons, (2) alcohol and alcohol metabolites are reinforcing within the mesolimbic dopamine system, (3) inhibiting the alcohol metabolic pathway inhibits the biological consequences of alcohol exposure, (4) alcohol consumption can be reduced by inhibiting/attenuating the alcohol metabolic pathway in the mesolimbic dopamine system, (5) alcohol metabolites can alter neurochemical levels within the mesolimbic dopamine system, and (6) alcohol interacts with alcohol metabolites to enhance the actions of both compounds. The data indicate that there is a positive relationship between alcohol and alcohol metabolites in regulating the biological consequences of consuming alcohol and the potential of alcohol use escalating to alcoholism.

show abstract

“…In addition, tobacco smoke contains other substances that have pharmacological effects, such as carbon monoxide, anabasine, acetaldehyde (Kunin, Latendresse, Gaskin, Smith, & Amit, 2000), and naphthoquinone (Castagnoli, Steyn, Petzer, Van der Schyf, & Castagnoli, 2001) that might be responsible for the monoamine oxidase inhibition seen in smokers (Fowler, Logan, Wang, & Volkow, 2003). Apart from these pharmacological factors, the sensory stimulation, package design, and behavioral features of tobacco and nicotine replacement product use differ and may contribute to the discrepancy in reinforcement power.…”

Section: Introductionmentioning

confidence: 99%

The nicotine market: An attempt to estimate the nicotine intake from various sources and the total nicotine consumption in some countries

Fagerström¹

2005

Nicotine & Tobacco Research

View full text Add to dashboard Cite

Tobacco--particularly smoked products--has been associated with great harm and growing public disapproval and can be expected to suffer in the marketplace. This situation has created opportunities for other less harmful nicotine-containing products such as smokeless tobacco and nicotine replacement products, which are gaining public support. Little is known about the level of nicotine intake in our society. Tobacco sales are known, but how much nicotine is extracted and actually absorbed by users is largely unknown. The present study is a first attempt to estimate uptake of nicotine from tobacco and nicotine replacement products and to map nicotine consumption in a few countries, with special emphasis on Sweden. Relevant pharmacokinetic studies for three types of nicotine-containing products (cigarettes, smokeless tobacco, and nicotine replacement products) were analyzed for bioavailable nicotine. Estimates of nicotine intake from each category were made. These were then multiplied by the amount consumed in the respective countries. Tobacco consumption statistics were usually from official records of taxed sales. In Sweden about 54% of all nicotine intake comes from smoked sources, 45% from nonsmoked tobacco, and 1.3% from nicotine replacement products. For men, 63% of the nicotine consumed comes from nonsmoked tobacco. Per-capita nicotine intake per year for adults aged 15 years or older is 3,321 mg for Austria, 3,043 mg for Sweden, 3,014 mg for Denmark, 2,955 mg for the United States, 2,244 mg for Norway, and 2,023 mg for Finland. Compared with cigarette smokers, snus users seem to have a somewhat higher daily intake (34 mg vs. 25 mg). The cleanest nicotine products, nicotine replacement products, represent a negligible part (about 1%) of the total nicotine consumption in most countries.

show abstract

Preexposure Effects of Nicotine and Acetaldehyde on Conditioned Taste Aversion Induced by Both Drugs

Cited by 19 publications

References 19 publications

Exposure to nicotine during periadolescence or early adulthood alters aversive and physiological effects induced by ethanol

Exposure to nicotine during periadolescence or early adulthood alters aversive and physiological effects induced by ethanol

Elucidating the biological basis for the reinforcing actions of alcohol in the mesolimbic dopamine system: the role of active metabolites of alcohol

The nicotine market: An attempt to estimate the nicotine intake from various sources and the total nicotine consumption in some countries

Contact Info

Product

Resources

About