Increases In Impulsive Choice Research Articles

Exercise Recovers Weight Gain, but Not Increased Impulsive Choice, Caused by a High-Fat Diet

A high-fat diet has negative effects on physical, neurological, and behavioral outcomes. One consistent finding is that a diet high in fat increases impulsive choice behavior—behavior that is linked to a wide range of other negative health behaviors. While the mechanism for this increase in impulsive choice is not well understood, exercise, with its well-known and many benefits, may serve as an effective and accessible way to combat increased impulsive choice associated with a high-fat diet. The goal of this work was to test this possibility. Rats were divided into four groups in a two-by-two factorial design: exercise and control diet, sedentary and control diet, exercise and high-fat diet, sedentary and high-fat diet. Rats in the exercise groups engaged in 30-min of forced, moderate intensity wheel-running exercise five days per week. Rats in the high-fat diet groups ate a diet high in fat. Impulsive choice was measured using a delay discounting task. Exercise prevented weight gain associated with the high-fat diet. Exercise also preserved relative motivation for food reinforcement. However, exercise did not prevent increases in impulsive choice observed for rats that consumed a high-fat diet relative to the rats that consumed the control diet. This work rules out several possible mechanisms by which a high-fat diet may increase impulsive choice behavior. It makes clear that exercise alone may not stave off increases in impulsive choice caused by a high-fat diet. Future work is necessary to uncover the underlying mechanism for this effect and discover interventions, perhaps ones that combine both physically and cognitively demanding activities, to improve health and behavior as it relates to decision making processes.

Exposure to Nicotine Vapor Produced by an Electronic Nicotine Delivery System Causes Short-Term Increases in Impulsive Choice in Adult Male Rats.

Traditional cigarette use influences cost-benefit decision making by promoting impulsive choice. However, the impact of nicotine exposure via electronic nicotine delivery systems on impulsivity remains unclear. Hence, the present study examined the short- and long-term effects of nicotine vapor on impulsive choice. Twenty-four adult male rats were trained in the delay discounting task to choose between small immediate food rewards and large delayed food rewards. After 24 days of training in the task rats were exposed to vapor containing either 0, 12, or 24 mg/mL of nicotine for 10 days. To validate inhalation of nicotine vapor serum cotinine levels were analyzed on exposure days 1, 5, and 10 using enzyme-linked immunosorbent assay. Following vapor exposure, rats were retrained in the discounting task until rats displayed stable responding and the effects of nicotine vapor on choice preference were assessed. Rats exposed to 12 and 24 mg/mL nicotine vapor displayed higher serum cotinine levels than control rats exposed to 0 mg/mL vapor. There were no differences in impulsive choice between any vapor exposure groups when tested 15 days after exposure, across 6 days of stable responding, suggesting that nicotine vapor does not have long lasting effects on impulsive choice. Interestingly, a subsequent nicotine vapor challenge revealed short-term increases in impulsive choice immediately following a single exposure to 24 mg/mL nicotine vapor, relative to choice preference immediately following exposure to 0 mg/mL vapor. These results suggest that exposure to nicotine vapor causes immediate, short-term increases in impulsive choice. E-cigarette use is increasing at an alarming rate, particularly among adolescents and young adults. This is concerning given the lack of research into the effects of nicotine vapor exposure on the brain and behavior. The present study describes a viable rodent model of human e-cigarette use and suggests that exposure to nicotine vapor produces short-term increases in impulsive choice.

Binge drinking and family history of alcoholism are associated with an altered developmental trajectory of impulsive choice across adolescence.

To test whether binge drinking, the density of familial alcoholism (FHD) and their interaction are associated with an altered developmental trajectory of impulsive choice across adolescence, and whether more life-time drinks are associated with a greater change in impulsive choice across age. Alcohol-naive adolescents, with varying degrees of FHD, were recruited as part of an ongoing longitudinal study on adolescent development, and were grouped based on whether they remained non-drinkers (n=83) or initiated binge drinking (n=33) during follow-up. During all visits, adolescents completed a monetary delay discounting task to measure impulsive choice. The effects of binge-drinking status, FHD and their interaction on impulsive choice across adolescence were tested. Developmental Brain Imaging Laboratory, Oregon Health & Science University, Portland, Oregon, USA. A total of 116 healthy male and female adolescents (ages 10-17 years at baseline) completed two to four visits between July 2008 and May 2016. Discounting rates were obtained based on adolescents' preference for immediate or delayed rewards. FHD was based on parent-reported prevalence of alcohol use disorder in the participant's first- and second-degree relatives. Binge-drinking status was determined based on the number of recent binge-drinking episodes. There was a significant interaction effect of binge-drinking status and FHD on impulsive choice across age (b=1.090, P<0.05, β=0.298). In adolescents who remained alcohol-naive, greater FHD was associated with a steeper decrease in discounting rates across adolescence (b=-0.633, P<0.05, β=-0.173); however, this effect was not present in binge-drinkers. Furthermore, total life-time drinks predicted escalated impulsive choice (b=0.002, P<0.05, β=0.295) in binge-drinking adolescents. A greater degree of familial alcoholism is associated with a steeper decline in impulsive choice across adolescence, but only in those who remain alcohol-naive. Meanwhile, more life-time drinks during adolescence is associated with increases in impulsive choice across age.

Effects of nucleus accumbens amphetamine administration on performance in a delay discounting task

Chronic administration of cocaine can cause pronounced and enduring cognitive alterations such as increases in impulsive choice. Chronic cocaine can also result in enhanced dopamine (DA) release in the nucleus accumbens (NAc) in response to reward-related cues. It is possible that this enhanced DA release in the NAc is a mechanism by which cocaine increases impulsive choice. To date, however, the specific role of DA in the NAc in impulsive choice is unclear. To begin to address this, rats received acute microinjections of the indirect DA agonist amphetamine directly into the NAc prior to testing in a delay discounting task in which rats chose between a small, immediate and a large, delayed food reward. When delays to the large reward increased within test sessions, amphetamine increased choice of the large reward. When delays decreased within test sessions, however, amphetamine decreased choice of the large reward. These findings suggest that, rather than specifically mediating impulsive choice, DA neurotransmission in the NAc is necessary for flexible adaptation of choice strategies in the presence of shifting reward contingencies. These results further indicate that enhancements in NAc DA release likely do not account for lasting increases in impulsive choice caused by chronic cocaine.

Intake-dependent effects of cocaine self-administration on impulsive choice in a delay discounting task.

Cocaine use is associated with high levels of impulsive choice (greater discounting of delayed rewards) in humans, but the cause/effect relationships between cocaine use and impulsive choice are not fully understood. In previous work, we found that both experimenter- and self-administration of fixed quantities of cocaine caused lasting increases in impulsive choice in rats. The present study extended these findings by taking into account baseline impulsive choice prior to self-administration and by allowing rats free access to cocaine. Male Long-Evans rats were trained in a delay discounting task in which they made discrete-trial choices between small immediate and large delayed food rewards. Half of the rats were then implanted with intravenous catheters and, following recovery, allowed to self-administer cocaine HCl (1.0 mg/kg/infusion) in 6-hr sessions over 14 days. Control rats orally self-administered a sucrose solution under similar conditions. Upon completion of self-administration, rats remained abstinent for 3 weeks before retesting in the delay discounting task. Cocaine and control groups did not differ prior to self-administration, but afterward, the cocaine group showed greater impulsive choice (fewer choices of large, delayed rewards) than controls. Additional analyses revealed that the effects of cocaine on impulsive choice were intake-dependent; rats classified as "low intake" did not differ from controls, whereas rats classified as "high intake" were significantly more impulsive than both controls and their precocaine baseline. These findings are consistent with the idea that cocaine-induced, pharmacologically based neural adaptations promote the development of impulsive decision making.

Baseline impulsive choice predicts the effects of nicotine and nicotine withdrawal on impulsivity in rats

Impulsive choice, a form of impulsivity, is associated with tobacco smoking in humans. Trait impulsivity may be a vulnerability factor for smoking, or smoking may lead to impulsive behaviors. We investigated the effects of 14-day nicotine exposure (6.32mg/kg/day base, subcutaneous minipumps) and spontaneous nicotine withdrawal on impulsive choice in low impulsive (LI) and high impulsive (HI) rats. Impulsive choice was measured in the delayed reward task in which rats choose between a small immediate reward and a large delayed reward. HI and LI rats were selected from the highest and lowest quartiles of the group before exposure to nicotine. In non-selected rats, nicotine or nicotine withdrawal had no effect on impulsive choice. In LI rats, chronic nicotine exposure decreased preference for the large reward with larger effects at longer delays, indicating increased impulsive choice. Impulsive choices for the smaller immediate rewards continued to increase during nicotine withdrawal in LI rats. In HI rats, nicotine exposure and nicotine withdrawal had no effect on impulsive choice, although there was a tendency for decreased preference for the large reward at short delays. These results indicate that nicotine- and nicotine withdrawal-induced increases in impulsive choice depend on trait impulsivity with more pronounced increases in impulsive choice in LI compared to HI subjects. Increased impulsivity during nicotine exposure may strengthen the addictive properties of nicotine and contribute to compulsive nicotine use.

Effects of acute and sub-chronic nicotine on impulsive choice in rats in a probabilistic delay-discounting task

Cigarette smokers typically display impulsivity by preferring immediate rewards over larger, delayed rewards at shorter delays than do non-smokers. Suggesting causality, nicotine injections in rats increase the choice for an immediate reward over a larger, delayed reward. To examine the generality of this latter effect, the present study employed a delay-discounting task to determine if acute and sub-chronic nicotine will also increase impulsive choice when subjective reward value is manipulated by changes in the probability, rather than magnitude, of reward. Rats were presented with two levers, one of which delivered an immediate water reward on half of the trials, while the other lever delivered the same reward on every trial, but only after one of five increasing delays. Acute injections of 1.2mg/kg, but not 0.8mg/kg, of nicotine increased the preference for the immediate (but less certain) reward lever at intermediate delays. Moreover, twice-daily injections of 0.8mg/kg of nicotine for 6days progressively increased the preference for the immediate reward. Latency to make the first response on each trial was not affected by nicotine. The similar increases in impulsive choice produced by both acute and sub-chronic nicotine in delay-discounting paradigms whether subjective reward value is manipulated by changes in reward magnitude or probability suggests that nicotine may be increasing what is common to these paradigms, namely delay discounting. Whatever the mechanism, these data indicate that both acute and sub-chronic nicotine may help develop and maintain an addiction by increasing impulsivity.

Nicotine and the behavioral mechanisms of intertemporal choice.

Nicotine has been found to produce dose-dependent increases in impulsive choice (preference for smaller, sooner reinforcers relative to larger, later reinforcers) in rats. Such increases could be produced by either of two behavioral mechanisms: (1) an increase in delay discounting (i.e., exacerbating the impact of differences in reinforcer delays) which would increase the value of a sooner reinforcer relative to a later one, or (2) a decrease in magnitude sensitivity (i.e., diminishing the impact of differences in reinforcer magnitudes) which would increase the value of a smaller reinforcer relative to a larger one. To isolate which of these two behavioral mechanisms was likely responsible for nicotine's effect on impulsive choice, we manipulated reinforcer delay and magnitude using a concurrent, variable interval (VI 30s, VI 30s) schedule of reinforcement with 2 groups of Long-Evans rats (n=6 per group). For one group, choices were made between a 1-s delay and a 9-s delay to 2 food pellets. For a second group, choices were made between 1 pellet and 3 pellets. Nicotine (vehicle, 0.03, 0.1, 0.3, 0.56 and 0.74 mg/kg) produced dose-dependent decreases in preference for large versus small magnitude reinforcers and had no consistent effect on preference for short versus long delays. This suggests that nicotine decreases sensitivity to reinforcer magnitude.

Self-administered cocaine causes long-lasting increases in impulsive choice in a delay discounting task.

Cocaine use is associated with high levels of impulsive choice (preference for immediate over delayed rewards), but it is not clear whether cocaine use causes elevated impulsive choice, or whether elevated impulsive choice is solely a predisposing factor for cocaine use. This study examined the effects of prior cocaine self-administration on rats performing a delay discounting task commonly used to measure impulsive choice. Male Long-Evans rats were implanted with intravenous catheters, and following recovery, were trained to self-administer 30 mg/kg/day cocaine HCl (approx. 0.5 mg/kg/infusion) for 14 consecutive days (a control group received yoked intravenous saline infusions). Following three weeks of withdrawal, all rats were food-restricted and began training on the delay discounting task in standard operant chambers. On each trial, rats were given a choice between two levers. A press on one lever delivered a small food reward immediately, and a press on the other delivered a large food reward after a variable delay period. Rats that self-administered cocaine displayed greater impulsive choice (enhanced preference for the small immediate over the large delayed reward, as reflected by shorter indifference points) compared to controls, but were no different from controls on a "probabilistic discounting" task in which they chose between small certain and large uncertain rewards. These data suggest that self-administered cocaine can cause lasting elevations in impulsive choice, and that the high levels of impulsive choice observed in human cocaine users may be due in part to long-term effects of cocaine on brain function.

Effects of chronic administration of drugs of abuse on impulsive choice (delay discounting) in animal models.

Drug-addicted individuals show high levels of impulsive choice, characterized by preference for small immediate over larger but delayed rewards. Although the causal relationship between chronic drug use and elevated impulsive choice in humans has been unclear, a small but growing body of literature over the past decade has shown that chronic drug administration in animal models can cause increases in impulsive choice, suggesting that a similar causal relationship may exist in human drug users. This article reviews this literature, with a particular focus on the effects of chronic cocaine administration, which have been most thoroughly characterized. The potential mechanisms of these effects are described in terms of drug-induced neural alterations in ventral striatal and prefrontal cortical brain systems. Some implications of this research for pharmacological treatment of drug-induced increases in impulsive choice are discussed, along with suggestions for future research in this area.

Cocaine exposure causes long-term increases in impulsive choice.

In this study, the authors examined the long-term effects of prior exposure to cocaine on a delay-discounting task commonly used to measure impulsive choice. Male Long-Evans rats received daily intraperitoneal injections of 30 mg/kg cocaine HCl or saline for 14 days. Following 3 weeks of withdrawal, rats began training. On each trial, rats were given a choice between 2 levers. A press on 1 lever resulted in immediate delivery of a single 45-mg food pellet, and a press on the other resulted in delivery of 4 pellets after a delay period. Impulsive choice was defined as preference for the small immediate over the large delayed reward. Three months after treatment, cocaine-exposed rats displayed increased impulsive choice behavior. They also showed less anticipatory responding (entries into the food trough) during the delays prior to reward delivery, indicating that the enhanced impulsive choice in these rats may be related to deficits in bridging the delay between response and reward. These data demonstrate that cocaine exposure can cause enduring increases in impulsive choice behavior, consistent with observations in human subjects with drug addictions.

Effects of acute and chronic nicotine on impulsive choice in rats

Impulsive choice, or preference for small immediate reinforcers over large delayed reinforcers, has been associated with cigarette smoking. The direct effects of nicotine on impulsive choice in laboratory animals are unknown. We examined the effects of acute and chronic nicotine injections, and the termination of injections, on impulsive choice in rats. Five rats made choices between a one- and a three-pellet reinforcer in a discrete trials procedure. The delay to the smaller reinforcer was always 1 s. A computer adjusted the delay to the larger reinforcer until the pattern of choices reflected indifference between the two alternatives. We assessed the effects of acute and chronic nicotine (vehicle, 0.03, 0.1, 0.3 and 1.0 mg/kg nicotine). The latency to make the first response of the session increased under the acute 1.0 mg/kg dose. There were no consistent differences in the effects of acute and chronic nicotine on response latency and lever pressing during the delays between choices. Acute injections of nicotine dose-dependently increased impulsive responding. After chronic injections, impulsive responding was increased equivalently regardless of dose, and it was increased even in the absence of nicotine. After drug injections were terminated, behavior remained impulsive for about 30 drug-free sessions, and then responding gradually returned to baseline levels. The results suggest that increases in impulsive choice were not due to anorectic effects, response biases or changes in conditioned reinforcement. Nicotine may have decreased the value of delayed reinforcers. Chronic nicotine exposure produced long-lasting but reversible increases in impulsive choice.