Reinforcer devaluation as a consequence of acute nicotine exposure and withdrawal

Kirshenbaum, Ari P.; Green, John T.; Parks, A. David; Phillips, Jesse; Stone, Jason D.; Roy, Tessa

doi:10.1007/s00213-014-3792-y

Cited by 11 publications

(10 citation statements)

References 71 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Mecamylamine abolished the nicotine REE at the highest dose tested (1 mg/kg), without altering response rates when given alone. The same overall result has previously been reported with both primary or conditioned reinforcers, studied with higher SC doses (i.e., 0.3-0.6 mg/kg) of nicotine (e.g., Guy and Fletcher 2013;Ivanová and Greenshaw 1997;Kirshenbaum et al 2014;Olausson et al 2004;Palmatier et al 2009). Mecamylamine, given at 1 mg/kg, would likely antagonize a variety of CNS and ganglionic nAChR subtypes (Papke et al 2001) but without inhibiting NMDA-type glutamate receptors (Clarke et al 1994).…”

Section: Individual Drugs and Receptor Targetssupporting

confidence: 76%

“…For example, enhancement of responding for brain stimulation reward and conditioned sensory reinforcers appears to depend on the participation of α4β2* nicotinic acetylcholine receptors (nAChRs) Spiller et al 2009;Tobey et al 2012) and several other transmitter systems (see Discussion). For primary sensory reinforcers, the focus of the present study, nicotine-induced enhancement is reported to be mimicked by the partial nAChR agonist varenicline (Levin et al 2012), abolished by the nAChR antagonist mecamylamine (Kirshenbaum et al 2014;Liu et al 2007;Palmatier et al 2009), reversed by the opioid antagonist naloxone (Kirshenbaum et al 2016), and unaffected by pretreatment with adrenergic or glutamatergic receptor antagonists (Palmatier et al 2009;Palmatier et al 2007).…”

Section: Introductionmentioning

confidence: 80%

See 1 more Smart Citation

Nicotine-induced enhancement of a sensory reinforcer in adult rats: antagonist pretreatment effects

et al. 2020

View full text Add to dashboard Cite

Rationale and objectives The reinforcement-enhancing effect (REE) of nicotine refers to the drug's ability to enhance the strength of other primary and conditioned reinforcers. The main aim was to investigate neuropharmacological mechanisms underlying nicotine's strengthening of a primary visual reinforcer (i.e., a light cue), using a subcutaneous (SC) dose previously shown to provide plasma nicotine levels associated with habitual smoking. Methods Adult male rats pressed an "active" lever to illuminate a brief cue light during daily 60-min sessions. Rats that showed a clear REE were tested with systemically administered pretreatment drugs followed by nicotine (0.1 mg/kg SC) or saline challenge, in within-subject counterbalanced designs. Pretreatments were mecamylamine (nicotinic, 0.1-1 mg/kg SC), SCH 39166 (D1-like dopaminergic, 0.003-0.2 mg/kg SC), naloxone (opioid, 1 and 5 mg/kg SC), prazosin (alpha1-adrenergic antagonist, 1 and 2 mg/kg IP), rimonabant (CB1 cannabinoid inverse agonist, 3 mg/kg IP), sulpiride (D2-like dopaminergic antagonist, 40 mg/kg SC), or propranolol (beta-adrenergic antagonist, 10 mg/kg IP). Results The nicotine REE was abolished by three antagonists at doses that did not impact motor output, i.e., mecamylamine (1 mg/kg), SCH 39166 (0.01 and 0.03 mg/kg), and naloxone (5 mg/kg). Prazosin and rimonabant both attenuated the nicotine REE, but rimonabant also suppressed responding more generally. The nicotine REE was not significantly altered by sulpiride or propranolol. Conclusions In adult male rats, the reinforcement-enhancing effect of low-dose nicotine depends on nicotinic receptor stimulation and on neurotransmission via D1/D5 dopaminergic, opioid, alpha1-adrenergic, and CB1 cannabinoid receptors.

show abstract

Section: Individual Drugs and Receptor Targetssupporting

confidence: 76%

Section: Introductionmentioning

confidence: 80%

Nicotine-induced enhancement of a sensory reinforcer in adult rats: antagonist pretreatment effects

et al. 2020

View full text Add to dashboard Cite

show abstract

“…In dependent smokers, forced abstinence is associated with diminished reward sensitivity (Dawkins, Powell, et al, 2007; Dawkins, Acaster, et al, 2007; Kalamboka et al, 2009; Lawn et al, 2015; Pergadia et al, 2014; Snuggs & Hajek, 2013), but whether the prolonged nicotine exposure that occurs in dependence is a necessary condition for reward desensitization to occur remains unclear. Unlike tests of the direct reinforcing-enhancement effect of nicotine, experimental evidence of reinforcement devaluation by nicotine (Kirshenbaum et al, 2015) in naïve users would require several nicotine doses over a substantially longer period in which to study nicotine’s aftereffects in the laboratory environment.…”

mentioning

confidence: 99%

Reinforcement enhancement by nicotine: A novel abuse-liability assessment of e-cigarettes in young adults.

Kirshenbaum

Hughes

2022

Experimental and Clinical Psychopharmacology

View full text Add to dashboard Cite

Nicotine can act as a primary positive reinforcer, and as negative reinforcer to relieve withdrawal; we tested whether it can also enhance the reinforcing efficacy of non-drug reinforcers. Young-adult never-users were delivered nicotine via e-cigarette, and a videogame reinforcer was used to test nicotine enhancement. Three dose groups were tested (placebo-only, 6 or 12-mg nicotine), and participants returned to the lab for several sessions over the course of 1 month. Those in the two nicotine-dose groups received placebo on some occasions and nicotine on others; nicotine enhancement of the videogame reinforcer was assessed in a within-subjects fashion by comparing each of the two nicotine groups' dedicated nicotine dose to placebo. In the placebo-only group, progressive-ratio (PR) schedule breakpoints did not alter as a function of videogame exposure, suggesting that the videogame retained its basic-reinforcing properties throughout the study. For the two groups that received nicotine, both doses of nicotine increased PR-schedule breakpoints for the videogame reinforcer relative to the placebo condition. Although nicotine was associated with greater subjective evaluation of the enjoyment of the videogame, it was unrelated to the enjoyment of the e-cigarette device. No evidence was found that nicotine elevated either anhedonia or withdrawal symptoms in the timeframe of the study. The results provide initial evidence that nicotine enhancement, via electronic cigarettes, occurs in non-frequent users of nicotine products and may be a reason they can develop nicotine dependence in the absence of withdrawal and direct effects of nicotine. Public Significance StatementOne reason e-cigarettes may have abuse liability is because the nicotine in them increases the reinforcing effects of non-drug rewards; these effects of nicotine are known as reinforcement-enhancement. We examined how nicotine contained in e-cigarettes changes video-game reinforcement in young-adult non-users, and how hedonic and subjective effects of nicotine are related to nicotine-induced reinforcement enhancement.

show abstract

“…Most studies to date have focused on the mechanisms and pathophysiology of chronic diseases caused by smoking [ 3 , 4 , 12 ]. However, acute exposure, defined as a single exposure to a harmful substance [ 25 ], is an important issue in adolescents who begin to smoke voluntarily [ 11 ]. Adolescents are more vulnerable to neurobiological changes, mental health, and substance-use disorders, as this period of life is essential for brain development associated with self-control and regulation [ 9 , 46 ].…”

Section: Introductionmentioning

confidence: 99%

Cardiovascular effects of linalyl acetate in acute nicotine exposure

Kim

Kang

Lee

et al. 2017

Environ Health Prev Med

View full text Add to dashboard Cite

BackgroudSmoking is a risk factor for cardiovascular diseases as well as pulmonary dysfunction. In particular, adolescent smoking has been reported to have a higher latent risk for cardiovascular disease. Despite the risk to and vulnerability of adolescents to smoking, the mechanisms underlying the effects of acute nicotine exposure on adolescents remain unknown. This study therefore evaluated the mechanism underlying the effects of linalyl acetate on cardiovascular changes in adolescent rats with acute nicotine exposure.MethodsParameters analyzed included heart rate (HR), systolic blood pressure, lactate dehydrogenase (LDH) activity, vascular contractility, and nitric oxide levels.ResultsCompared with nicotine alone, those treated with nicotine plus 10 mg/kg (p = 0.036) and 100 mg/kg (p = 0.023) linalyl acetate showed significant reductions in HR. Moreover, the addition of 1 mg/kg (p = 0.011), 10 mg/kg (p = 0.010), and 100 mg/kg (p = 0.011) linalyl acetate to nicotine resulted in significantly lower LDH activity. Nicotine also showed a slight relaxation effect, followed by a sustained recontraction phase, whereas nicotine plus linalyl acetate or nifedipine showed a constant relaxation effect on contraction of mouse aorta (p < 0.001). Furthermore, nicotine-induced increases in nitrite levels were decreased by treatment with linalyl acetate (p < 0.001).ConclusionsTaken together, our findings suggest that linalyl acetate treatment resulted in recovery of cell damage and cardiovascular changes caused by acute nicotine-induced cardiovascular disruption. Our evaluation of the influence of acute nicotine provides potential insights into the effects of environmental tobacco smoke and suggests linalyl acetate as an available mitigating agent.

show abstract

Reinforcer devaluation as a consequence of acute nicotine exposure and withdrawal

Cited by 11 publications

References 71 publications

Nicotine-induced enhancement of a sensory reinforcer in adult rats: antagonist pretreatment effects

Nicotine-induced enhancement of a sensory reinforcer in adult rats: antagonist pretreatment effects

Reinforcement enhancement by nicotine: A novel abuse-liability assessment of e-cigarettes in young adults.

Cardiovascular effects of linalyl acetate in acute nicotine exposure

Contact Info

Product

Resources

About