Abstract

While the cognitive enhancing effects of nicotine use have been well documented, it has also been shown to impair decision making. The goal of this study was to determine if exposure to nicotine vapor increases risky decision making. The study also aims to investigate possible long-term effects of nicotine vapor exposure on the expression of genes coding for cholinergic and dopaminergic receptors in brain. Thirty-two adult male Sprague Dawley rats were exposed to 24 mg/mL nicotine vapor or vehicle control, immediately followed by testing in the probability discounting task for 10 consecutive days. Fifty-four days after the 10-day vapor exposure, animals were sacrificed and expression of genes coding for the α4 and β2 cholinergic receptor subunits, and dopamine D1 and D2 receptors, were analyzed using RT-PCR. Exposure to nicotine vapor caused an immediate and transient increase in risky choice. Analyses of gene expression identified significant reductions in CHRNB2 and DRD1 in the nucleus accumbens core and CHRNB2 and DRD2 in the medial prefrontal cortex of rats previously exposed to nicotine vapor, relative to vehicle controls. Results provide data on the negative cognitive effects of nicotine vapor exposure and identify cholinergic and dopaminergic mechanisms that may affected with repeated use.

Highlights

  • As previously observed in our laboratory, a repeated measures analysis of variance (ANOVA) revealed a main effect of day (F(1,31) = 9.97, p < 0.01, η p 2 = 0.86) and a main effect of block (F(3,93) = 246.79, p < 0.01, η p 2 = 1.00), with no interaction of day and block (F(3,93) = 2.02, p = 0.12), when comparing risky choice on nicotine vehicle exposure day 1 to average risky choice on

  • The goal of the present study was to examine the ability of nicotine vapor exposure shift risky choice, as determined by the probabilistic discounting task, in adult male rats

  • Findings from this study provide much need data on the effects of nicotine vapor exposure on risky decision making and the mechanisms that drive choice

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Summary

Introduction

Successful commercial development of electronic cigarettes (commonly referred to as e-cigarettes) occurred in 2003. While they were originally developed as tool for smoking cessation, recreational use of e-cigarettes has increased at an alarming rate, within the adolescent population [1]. Clinical studies investigating e-cigarette use have linked repeated nicotine vapor inhalation with negative health consequences that can differ from those produced from tobacco leaf smoke inhalation [2,3]. Preclinical studies have begun to shed light on the toxic health effects of e-cigarettes, including the negative impact on the brain and behavior [4,5,6]. Research has shown that relative to tobacco leaf cigarettes, e-cigarettes expose users to distinct nicotine concentrations, chemical additives (e.g., salt, flavorings), and chemical reaction products (e.g., nicotyrine) that enhance nicotine’s rewarding properties and promote a transition to tobacco leaf cigarette use in individuals with no history of smoking [7,8,9,10]

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