Drug cue induced overshadowing: selective disruption of natural reward processing by cigarette cues amongst abstinent but not satiated smokers

Freeman, Tanya; Morgan, Candia; Beesley, Tom; Curran, H. Valerie

doi:10.1017/s0033291711001139

Cited by 29 publications

(33 citation statements)

References 49 publications

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“…More generally, on-line iterative reinforcement learning in which behaviour (and hence sampling of the environment) changes after every experience often does not have the kind of optimality guarantees that off-line learning has (Bertsekas and Tsitsiklis, 1996), and may lead to self-reinforcing loops of choice and reward (Hogarth et al, 2007). One such effect was shown directly by Freeman et al (2012), who have found that abstinent smokers were more likely to associate a drug cue with reward than a non-drug cue. Indeed, attentional mechanisms are clearly important in learning (Pearce, 1997;Dayan et al, 2000) and possibly in the maintenance of addiction (Hogarth and Chase, 2011;Hogarth et al, 2013;Wiers et al, 2011).…”

Section: Individual Variability In Addiction Vulnerabilitymentioning

confidence: 99%

The role of learning-related dopamine signals in addiction vulnerability

Huys

Tobler

Hasler

et al. 2014

Progress in Brain Research

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Psychostimulants such as methylphenidate (MPH) and antidepressants such as fluoxetine (FLX) are widely used in the treatment of various mental disorders or as cognitive enhancers. These medications are often combined, for example, to treat comorbid disorders. There is a considerable body of evidence from animal models indicating that individually these psychotropic medications can have detrimental effects on the brain and behavior, especially when given during sensitive periods of brain development. However, almost no studies investigate possible interactions between these drugs. This is surprising given that their combined neurochemical effects (enhanced dopamine and serotonin neurotransmission) mimic some effects of illicit drugs such as cocaine and amphetamine. Here, we summarize recent studies in juvenile rats on the molecular effects in the mid-and forebrain and associated behavioral changes, after such combination treatments. Our findings indicate that these combined MPH + FLX treatments can produce similar molecular changes as seen after cocaine exposure while inducing behavioral changes indicative of dysregulated mood and motivation, effects that often endure into adulthood. Tables: 2 References: 254 ABSTRACT Dopaminergic signals play a mathematically precise role in reward-related learning, and variations in dopaminergic signalling have been implicated in vulnerability to addiction. Here, we provide a detailed overview of the relationship between theoretical, mathematical and experimental accounts of phasic dopamine signalling, with implications for the role of learning-related dopamine signalling in addiction and related disorders. We describe the theoretical and behavioural characteristics of model-free learning based on errors in the prediction of reward, including step-by-step explanations of the underlying equations. We then use recent insights from an animal model that highlights individual variation in learning during a Pavlovian conditioning paradigm to describe overlapping aspects of incentive salience attribution and model-free learning. We argue that this provides a computationally coherent account of some features of addiction. CONTENTS

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Section: Individual Variability In Addiction Vulnerabilitymentioning

confidence: 99%

The role of learning-related dopamine signals in addiction vulnerability

Huys

Tobler

Hasler

et al. 2014

Progress in Brain Research

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“…This excessive effect of smoking cues on neural activation was shown to be modulated by genes related to the dopamine transporter [89] and to be reduced by administration of varenicline, a smoking cessation medication that functions as a partial agonist of nicotinic receptors [90]. An attentional bias toward smoking cues was also identified in abstinent smokers, which was related to activation in DLPFC, putamen, posterior cingulate cortex and primary motor cortex [91] and was shown to overshadow the value of neutral cues predicting natural reward [92]. Finally, the neural response to smoking cues compared to the neural activation to pleasant stimuli was shown to be predictive of abstinence [93].…”

Section: Findings In Human Smokersmentioning

confidence: 99%

“…An attentional bias toward smoking cues was also identified in abstinent smokers, which was related to activation in DLPFC, putamen, posterior cingulate cortex and primary motor cortex [91] and was shown to overshadow the value of neutral cues predicting natural reward [92]. Finally, the neural response to smoking cues compared to the neural activation to pleasant stimuli was shown to be predictive of abstinence [93]. …”

Section: Findings In Human Smokersmentioning

confidence: 99%

Neuroadaptive Changes Associated with Smoking: Structural and Functional Neural Changes in Nicotine Dependence

Martin‐Soelch

2013

Brain Sciences

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Tobacco smoking is the most frequent form of substance abuse. We provide a review of the neuroadaptive changes evidenced in human smokers with regard to the current neurobiological models of addiction. Addiction is thought to result from an interplay between positive and negative reinforcement. Positive reinforcing effects of the drugs are mediated by striatal dopamine release, while negative reinforcement involves the relief of withdrawal symptoms and neurobiological stress systems. In addition, drug-related stimuli are attributed with excessive motivational value and are thought to exert a control on the behavior. This mechanism plays a central role in drug maintenance and relapse. Further neuroadaptive changes associated with chronic use of the drug consist of reduced responses to natural rewards and in the activation of an antireward system, related to neurobiological stress systems. Reduced inhibitory cognitive control is believed to support the development and the maintenance of addiction. The findings observed in human nicotine dependence are generally in line with these models. The current state of the research indicates specific neuroadaptive changes associated with nicotine addiction that need to be further elucidated with regard to their role in the treatment of nicotine dependence.

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“…Abstinent smokers demonstrate increased desire to smoke (i.e. craving) (Shiffman and Jarvik 1976), along with diminished interested in pleasant events, evidenced by decreased attentional bias toward positive stimuli (Dawkins et al 2006; Freeman et al 2012; Leventhal et al 2012; Powell et al 2002b; Powell et al 2004); lower ratings of attractiveness for unfamiliar faces (Attwood et al 2009); lower ratings of anticipated enjoyment in activities; and reduced responsiveness to monetary reward (Dawkins et al 2006; Geier et al 2014; Powell et al 2002a; Powell et al 2004). Consistent with behavioral evidence, we recently demonstrated that 24 hr abstinence from smoking—compared with smoking as usual—was associated with both heightened response to smoking reward (i.e., puffs of a cigarette delivered after the scan) and attenuated response to monetary reward within the ventral striatum (Sweitzer et al 2013b)—a key component of reward circuitry thought to encode motivational salience of primary and secondary reinforcers (Bassareo and Di Chiara 1999; Delgado et al 2000; O’Doherty 2004; Schultz 2000).…”

Section: Introductionmentioning

confidence: 99%

Blunted striatal response to monetary reward anticipation during smoking abstinence predicts lapse during a contingency-managed quit attempt

et al. 2015

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Rationale Tobacco smoking is associated with dysregulated reward processing within the striatum, characterized by hypersensitivity to smoking rewards and hyposensitivity to non-smoking rewards. This bias toward smoking reward at the expense of alternative rewards is further exacerbated by deprivation from smoking, which may contribute to difficulty maintaining abstinence during a quit attempt. Objective We examined whether abstinence-induced changes in striatal processing of rewards predicted lapse likelihood during a quit attempt supported by contingency management (CM), in which abstinence from smoking was reinforced with money. Methods Thirty-six non-treatment seeking smokers participated in two fMRI sessions, one following 24-hr abstinence and one following smoking as usual. During each scan, participants completed a rewarded guessing task designed to elicit striatal activation in which they could earn smoking and monetary rewards delivered after the scan. Participants then engaged in a 3-week CM-supported quit attempt. Results As previously reported, 24-hr abstinence was associated with increased striatal activation in anticipation of smoking reward and decreased activation in anticipation of monetary reward. Individuals exhibiting greater decrements in right striatal activation to monetary reward during abstinence (controlling for activation during non-abstinence) were more likely to lapse during CM (p<.05), even when controlling for other predictors of lapse outcome (e.g., craving); no association was seen for smoking reward. Conclusions These results are consistent with a growing number of studies indicating the specific importance of disrupted striatal processing of non-drug reward in nicotine dependence, and highlight the importance of individual differences in abstinence-induced deficits in striatal function for smoking cessation.

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Drug cue induced overshadowing: selective disruption of natural reward processing by cigarette cues amongst abstinent but not satiated smokers

Abstract: These findings provide the first evidence that drug cues interact with reward processing in a drug dependent population.

Cited by 29 publications

References 49 publications

The role of learning-related dopamine signals in addiction vulnerability

The role of learning-related dopamine signals in addiction vulnerability

Neuroadaptive Changes Associated with Smoking: Structural and Functional Neural Changes in Nicotine Dependence

Blunted striatal response to monetary reward anticipation during smoking abstinence predicts lapse during a contingency-managed quit attempt

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