Nicotine and methamphetamine disrupt habituation of sensory reinforcer effectiveness in male rats.

Lloyd, D. R.; Hausknecht, Kathryn A.; Richards, Jerry B.

doi:10.1037/a0034741

Cited by 13 publications

(18 citation statements)

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“…That said, nicotine also enhanced the responding for an unpaired stimulus, which reflects the possibility that nicotine enhances the reinforcing properties of stimuli that have not been paired with reward as well, such as has been shown by others (Palmatier et al 2013). The initial reinforcing properties of these stimuli are likely to be important for this effect, because nicotine and other stimulants may disrupt the habituation to the sensory reinforcement maintained by a variety of stimuli (Lloyd et al 2012; 2014a; 2014b). …”

Section: Discussionmentioning

confidence: 99%

The tendency to sign-track predicts cue-induced reinstatement during nicotine self-administration, and is enhanced by nicotine but not ethanol

2016

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Rationale Some individuals are particularly responsive to reward-associated stimuli (“cues”), including the effects of these cues on craving and relapse to drug-seeking behavior. In the cases of nicotine and alcohol, cues may acquire these abilities via the incentive-enhancing properties of the drug. Objectives To determine the interaction between cue-responsivity and nicotine reinforcement, we studied the patterns of nicotine self-administration in rats categorized based on their tendency to approach a food predictive cue (“sign-trackers”) or a reward-delivery location (“goal-trackers”). In a second experiment, we determined whether nicotine and ethanol altered the incentive value of a food cue. Methods Rats were classified as sign- or goal-trackers during a Pavlovian conditioned approach paradigm. Rats then self-administered intravenous nicotine (0.03 mg/kg infusions) followed by extinction and cue induced reinstatement tests. We also tested the effects of nicotine (0.4 mg/kg base s.c.) or ethanol (0.7 g/kg i.p.) on the approach to, and reinforcing efficacy of, a food cue. Results Sign-trackers showed greater reinstatement in response to a nicotine cue. Further, nicotine enhanced sign-tracking but not goal-tracking to a food cue, and also enhanced responding for the food cue during the conditioned reinforcement test. Conversely, ethanol reduced sign-tracking and increased goal-tracking, but had no effect on conditioned reinforcement. Conclusions Our studies demonstrate that the tendency to attribute incentive value to a food cue predicts enhanced cue-induced reinstatement. Additionally, the incentive value of food cues is differentially modulated by nicotine and ethanol, which may be related to the reinforcing effects of these drugs.

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Section: Discussionmentioning

confidence: 99%

The tendency to sign-track predicts cue-induced reinstatement during nicotine self-administration, and is enhanced by nicotine but not ethanol

2016

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“…10,11 In the OSS assay, robust within-session habituation to the reinforcing effects of purely visual stimuli has been observed. 10,11 In the OSS assay, robust within-session habituation to the reinforcing effects of purely visual stimuli has been observed.…”

Section: Genome-wide Significant Qtl On Chromosomes 4 and 13 Are Asmentioning

confidence: 99%

“…[10][11][12] In this regard, an intriguing hypothesis is that heritable variation in the homeostatic set point of sensory stimulation 13 underlies the observed relationship between sensation seeking and substance use in humans, and that these fundamental biological mechanisms are conserved across species. A complementary approach is to measure an intermediate sensation seeking phenotype that (a) directly indexes the fundamental psychological drive that is shared by sensation seeking and substance use, (b) allows dissociation of biological mechanisms affecting motoric behaviors from those affecting sensation seeking and drug use and (c) is directly comparable across species.…”

Section: Introductionmentioning

confidence: 99%

Systems genetics of sensation seeking

Dickson

Roy

McNaughton

et al. 2018

Genes Brain and Behavior

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Sensation seeking is a multifaceted, heritable trait which predicts the development of substance use and abuse in humans; similar phenomena have been observed in rodents. Genetic correlations among sensation seeking and substance use indicate shared biological mechanisms, but the genes and networks underlying these relationships remain elusive. Here, we used a systems genetics approach in the BXD recombinant inbred mouse panel to identify shared genetic mechanisms underlying substance use and preference for sensory stimuli, an intermediate phenotype of sensation seeking. Using the operant sensation seeking (OSS) paradigm, we quantified preference for sensory stimuli in 120 male and 127 female mice from 62 BXD strains and the C57BL/6J and DBA/2J founder strains. We used relative preference for the active and inactive levers to dissociate preference for sensory stimuli from locomotion and exploration phenotypes. We identified genomic regions on chromosome 4 (155.236-155.742 Mb) and chromosome 13 (72.969-89.423 Mb) associated with distinct behavioral components of OSS. Using publicly available behavioral data and mRNA expression data from brain regions involved in reward processing, we identified (a) genes within these behavioral QTL exhibiting genome-wide significant cis-eQTL and (b) genetic correlations among OSS phenotypes, ethanol phenotypes and mRNA expression. From these analyses, we nominated positional candidates for behavioral QTL associated with distinct OSS phenotypes including Gnb1 and Mef2c. Genetic covariation of Gnb1 expression, preference for sensory stimuli and multiple ethanol phenotypes suggest that heritable variation in Gnb1 expression in reward circuitry partially underlies the widely reported relationship between sensation seeking and substance use.

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“…Preclinical research shows that nicotine (and methamphetamine) slows habituation of the reinforcing effectiveness of a visual reward (87). Such an effect may be more pronounced for rewards that are intermediate in reinforcing efficacy between those extremely desired versus minimally desired, which may produce very slow versus very fast habituation, respectively (88).…”

Section: Potential Clinical Implicationsmentioning

confidence: 99%

Nicotine Acutely Enhances Reinforcement from Non-Drug Rewards in Humans

Perkins¹,

Karelitz²,

Boldry³

2017

Front. Psychiatry

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Preclinical research documents that, aside from the primary and secondary reinforcing effects of nicotine intake itself, nicotine also acutely enhances the reinforcing efficacy of non-drug reinforcers ("rewards"). Study of these effects in humans has largely been overlooked, but very recent findings suggest they may have clinical implications for more fully understanding the persistence of tobacco dependence. This overview first outlines the topic and notes some recent human studies indirectly addressing nicotine effects on related responses (e.g., subjective ratings), explaining why those findings do not directly confirm enhancement of behavioral reinforcement per se due to nicotine. Then, the methodology used in the subsequently presented studies is described, demonstrating how those studies specifically did demonstrate enhancement of reinforced responding for non-drug rewards. The main section focuses on the limited controlled research to date directly assessing nicotine's acute reinforcement-enhancing effects in humans, particularly as it relates to reinforced behavioral responding for non-drug rewards in non-human animal models. After detailing those few existing human studies, we address potential consequences of these effects for dependence and tobacco cessation efforts and then suggest directions for future research. This research indicates that nicotine per se increases responding in humans that is reinforced by some rewards (auditory stimuli via music, visual stimuli via video), but perhaps not by others (e.g., money). These reinforcement-enhancing effects in smokers are not due to dependence or withdrawal relief and can be restored by a small amount of nicotine (similar to a smoking lapse), including from e-cigarettes, a non-tobacco nicotine product. Future clinical research should examine factors determining which types of rewards are (or are not) enhanced by nicotine, consequences of the loss of these nicotine effects after quitting smoking, potential individual differences in these effects, and the possibility that nicotine via nicotine replacement therapy and non-nicotine quit medications may attenuate loss of these effects upon quitting. Further study with humans of nicotine's reinforcement-enhancing effects may provide a more complete understanding of smoking persistence and added mechanisms of cessation medication efficacy.

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Nicotine and methamphetamine disrupt habituation of sensory reinforcer effectiveness in male rats.

Cited by 13 publications

References 50 publications

The tendency to sign-track predicts cue-induced reinstatement during nicotine self-administration, and is enhanced by nicotine but not ethanol

The tendency to sign-track predicts cue-induced reinstatement during nicotine self-administration, and is enhanced by nicotine but not ethanol

Systems genetics of sensation seeking

Nicotine Acutely Enhances Reinforcement from Non-Drug Rewards in Humans

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