Exposure to nicotine vapor causes short-term increases in impulsive choice in rats (original) (raw)
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Behavioural Pharmacology, 2010
Biological differences may underlie individual differences in impulsive behavior, such as choice for a smaller, more immediate reinforcer over a larger, more delayed reinforcer. Repeated exposure to drugs of abuse may have differing effects on such behavior. To evaluate acute and repeated effects of nicotine on impulsive choice, two strains of rats that have been shown to differ in impulsive choice were tested in a delay-discounting paradigm. Eight Lewis and eight Fischer 344 rats were allowed to choose between one food pellet delivered immediately and three food pellets delivered after a delay. The delay systematically increased in blocks of trials within each session, and the delay value at which choice for the two alternatives was equal (i.e., the indifference point) was interpolated. Effects of nicotine (0.1-1.0 mg/kg, s.c.) on percent choice and indifference points were determined during the acute-testing phase and during the redetermination of effects of each dose following at least 30 sessions of repeated 1.0 mg/kg nicotine exposure. Lewis rats had shorter indifference points (i.e., made fewer larger reinforcer choices) than the Fischer 344 rats. Acute nicotine administration increased mean larger-reinforcer choices at the 0.3 mg/kg dose in the Lewis rats and at the 1.0 mg/kg dose in the Fischer 344 rats. After repeated exposure to nicotine, indifference points returned to near baseline (pre-drug) levels for both strains. Strain differences were observed in rates of delay discounting and nicotine may decrease impulsive choice acutely, but this effect does not appear to be long-lasting.
Effects of developmental nicotine exposure in rats on decision-making in adulthood
Behavioural Pharmacology, 2012
Exposure to tobacco smoke during pregnancy is associated with a range of adverse Outcomes in offspring, including cognitive deficits and increased incidence of attention deficit-hyperactivity disorder (ADHD), but there is considerable controversy concerning the causal role of tobacco smoke in these outcomes. To determine whether developmental exposure to the primary psychoactive ingredient in tobacco smoke, nicotine, may cause long-lasting behavioral alterations analogous to those in ADHD, male Sprague-Dawley rats underwent a chronic neonatal nicotine administration regimen which models third-trimester human exposure. Male rat pups were administered nicotine (6 mg/kg/day) by oral gastric intubation on postnatal days 1-7. In adulthood, rats were tested in two decision-making tasks (risky decision making and delay discounting) as well as in free-operant responding for food reward and the elevated plus maze (EPM). Chronic neonatal nicotine attenuated weight gain during nicotine exposure, but there were no effects on performance in either decision-making task, and only a modest decrease in arm entries in the EPM in one subgroup of rats. These data are consistent with previous findings that developmental nicotine exposure has no effect on delay-discounting, and they extend these findings to risky decision making as well. They further suggest that at least some neurocognitive alterations associated with prenatal tobacco smoke exposure in humans may be due to genetic or other environmental factors, including non-nicotine components of tobacco smoke.
Journal of the Experimental Analysis of Behavior, 2009
Many drugs of abuse produce changes in impulsive choice, that is, choice for a smaller-sooner reinforcer over a larger-later reinforcer. Because the alternatives differ in both delay and amount, it is not clear whether these drug effects are due to the differences in reinforcer delay or amount. To isolate the effects of delay, we used a titrating delay procedure. In phase 1, 9 rats made discrete choices between variable delays (1 or 19 s, equal probability of each) and a delay to a single food pellet. The computer titrated the delay to a single food pellet until the rats were indifferent between the two options. This indifference delay was used as the starting value for the titrating delay for all future sessions. We next evaluated the acute effects of nicotine (subcutaneous 1.0, 0.3, 0.1, and 0.03 mg/kg) on choice. If nicotine increases delay discounting, it should have increased preference for the variable delay. Instead, nicotine had very little effect on choice. In a second phase, the titrated delay alternative produced three food pellets instead of one, which was again produced by the variable delay (1 s or 19 s) alternative. Under this procedure, nicotine increased preference for the one pellet alternative. Nicotine-induced changes in impulsive choice are therefore likely due to differences in reinforcer amount rather than differences in reinforcer delay. In addition, it may be necessary to include an amount sensitivity parameter in any mathematical model of choice when the alternatives differ in reinforcer amount.
Effects of Acute Nicotine on Several Operant Behaviors in Rats
Pharmacology Biochemistry and Behavior, 2000
Effects of acute nicotine on several operant behaviors in rats. PHARMACOL BIOCHEM BEHAV 65 (2) 247-254, 2000.-The present experiment assessed nicotine's effects on complex cognitive processes using a variety of operant tasks in rats, including incremental repeated acquisition (IRA) to assess learning; conditioned position responding (CPR) to assess auditory, visual, and position discrimination; progressive ratio (PR) to assess motivation; temporal response differentiation (TRD) to assess timing; and differential reinforcement of low response rates (DRL) to assess timing and response inhibition. Acute nicotine administration (0.0, 0.3, 0.42, 0.56, 0.75, and 1.0 mg/kg, IP) increased IRA and CPR response rate without significantly altering accuracy. Nicotine had similar effects on response rate for PR. For TRD, nicotine had a U-shaped dose effect on accuracy, but failed to shift the mode of the TRD response distribution. For DRL, nicotine reduced accuracy and also shifted the mode of the DRL response initiation time distribution to the left. Nicotine produced an inverted U-shaped dose-effect curve for the overall number of "bursting" responses under both of these schedules. The results of this experiment suggest that nicotine can impair performance on some aspects of cognitive-behavioral performance, while simultaneously improving performance on others. © 2000 Elsevier Science Inc.
Nicotine-induced impulsive action
Behavioural Pharmacology, 2011
A conjunctive variable-interval differential-reinforcement-of-low-rate (VI-DRL, n= 18) responding schedule and a stop-signal task (n= 18) were used to evaluate the disinhibiting effects of nicotine on response withholding in rats. Sucrose solution was used to reinforce responding, and after a stable baseline was achieved under saline-administration conditions, 0.3 mg/kg nicotine was delivered before each session. Experiment 1 showed that repeated, but not the initial, administration of nicotine decreased performance on both tasks, and the effect of sensitization followed a similar timeline; 10 consecutive doses resulted in poorer proportion-correct VI-DRL trials and percent correct stop trials than the initial dose of nicotine. Furthermore, sensitization to 0.3 mg/kg nicotine decreased performance regardless of whether a spaced or consecutive-dosing regimen was followed. Experiment 2 was designed to test whether mecamylamine hydrochloride (0.1-1.0 mg/kg) could attenuate the effects of repeated 0.3 mg/kg nicotine administration, and the degree to which mecamylamine attenuation of the effect of nicotine to produce impulsive action was relative to dose. Results from experiment 2 showed that response disinhibition, as evaluated using the VI-DRL and stop-signal tasks, is related in a systematic manner to nicotinicacetylcholine receptor activation.
Neurochemical mechanisms mediating the behavioral and cognitive effects of nicotine
Drug Development Research, 1994
Data are reviewed, largely from experiments in the authors'laboratory, that suggest three modes of action of systemic nicotine in producing three different types of effect upon behavior and cognitive function. (1) Preexposure of a stimulus without consequence makes it harder subsequently to form associations to that stimulus, a form of selective attention known as latent inhibition. Latent inhibition is blocked by nicotine, an effect that is apparently mediated by a nicotine‐induced increase in dopamine release in the nucleus accumbens. (2) A single dose of nicotine proactively increases the partial reinforcement extinction effect measured several weeks later: that is, resistance to extinction is decreased by nicotine in animals that have been trained on a continuous reinforcement schedule, and increased in animals trained on a partial reinforcement schedule. This effect appears to be due to increased synthesis of tyrosine hydroxylase in the cell bodies of noradrenergic neurons ...
Rodent models of nicotine reward: What do they tell us about tobacco abuse in humans?
Pharmacology Biochemistry and Behavior, 2009
Tobacco products are widely abused in humans, and it is assumed that nicotine is the key substrate in these products that produces addiction. Based on this assumption, several pre-clinical studies have utilized animal models to measure various aspects of nicotine addiction. Most of this work has focused on behavioral measures of nicotine and how other variables contribute to these effects. Here we discuss the most commonly used animal models including, self-administration (SA), place conditioning (PC), and the intracranial self-stimulation (ICSS) paradigms in rodents. The strengths, limitations and procedural variables of these models are reviewed, followed by a discussion of how the animal models have been used to study factors such as age, sex, stress, and the effects of tobacco products other than nicotine. These factors are discussed in light of their influences on human tobacco abuse. The rodent models are evaluated in the context of face, predictive, and construct validity, and we propose that inclusion of factors such as age, sex, stress and other constituents of tobacco aside from nicotine can increase the utility of these animal models by more closely mimicking human tobacco abuse.
Increased Risky Choice and Reduced CHRNB2 Expression in Adult Male Rats Exposed to Nicotine Vapor
International Journal of Molecular Sciences, 2022
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 nu...
2022
In recent years, there has been a dramatic increase in nicotine vapor consumption via electronic nicotine delivery systems (i.e., e-cigarettes), particularly in adolescents. While recent work has focused on the health effects of nicotine vapor exposure, its effects on the brain and behavior remain unclear. In this study, we assessed the effects that cessation from repeated nicotine vapor exposure had on behavioral and neuronal measures of withdrawal. For Experiment 1, fifty-six adult male rats were tested for plasma cotinine levels, somatic withdrawal signs, and anxiety-like behavior in the elevated plus maze, immediately following precipitated withdrawal from repeated exposure to 12 or 24 mg/mL nicotine vapor. In Experiment 2, twelve adult male rats were tested for intracranial self-stimulation (ICSS) across 14 days of exposure to 24 mg/mL nicotine vapor and across the 14 days immediately following nicotine exposure. Results revealed that plasma cotinine, somatic signs, anxiety-lik...
Effect of impulsivity on craving and behavioral reactivity to smoking cues
Psychopharmacology, 2007
Introduction Nearly 25% of American adults remain regular smokers. Current smokers may be especially likely to possess characteristics that impair their ability to quit, such as impulsivity. Impulsive individuals may be overly prone to smoke because they are particularly drawn to rewarding stimuli and related cues. The aim of this study was to test the hypothesis that more impulsive smokers are more responsive to cigarette cues than other smokers. Materials and methods In a repeated measures design, 60 euthymic, adult smokers (50% female) were exposed to a smoking cue and a neutral cue in two experimental sessions. Cue reactivity was operationalized as changes in cigarette craving and preference for immediate vs delayed smoking after cue exposure. Results Impulsivity predicted a heightened craving response to both cues but particularly the smoking cue (t [161] = 3.21, p = 0.002). Smokers with high levels of impulsivity exhibited a greater preference for immediate rewards over larger, delayed rewards in terms of both hypothetical (t [58] = 5.99, p = 0.001) and actual (z = 3.02, p = 0.003) rewards. Conclusion These data suggest that increased reactivity to environmental smoking cues contributes to the link between impulsivity and smoking.