ArticlePsychopharmacology2015
Reinforcer devaluation as a consequence of acute nicotine exposure and withdrawal.
Article in Psychopharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Reinforcement enhancement by nicotine: A novel abuse-liability assessment of e-cigarettes in young adults.Experimental and clinical psychopharmacology · 2022Article
- Stimulus functions of nicotine.Advances in pharmacology (San Diego, Calif.) · 2022Article
- Nicotine-induced enhancement of a sensory reinforcer in adult rats: antagonist pretreatment effects.Psychopharmacology · 2021Article
- Precipitated Δ9-THC withdrawal reduces motivation for sucrose reinforcement in mice.Pharmacology, biochemistry, and behavior · 2020Article
- Cardiovascular effects of linalyl acetate in acute nicotine exposure.Environmental health and preventive medicine · 2017Article
- The effects of nicotine self-administration and withdrawal on concurrently available chow and sucrose intake in adult male rats.Physiology & behavior · 2016Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
rationaleNicotine discontinuation produces behaviors in rats that are congruent with anhedonia, and these symptoms may be related to the devaluation of non-nicotine reinforcers.
objectiveFour separate experiments were performed to explore the parameters surrounding nicotine-induced reinforcer devaluation.
methodsIn Experiments 1 and 2, nicotine (0.1 or 0.3 mg/kg) or 0.3 mg/kg nicotine plus 1.0 mg/kg mecamylamine was delivered to rats prior to progressive ratio (PR) schedule sessions in which sucrose was used as a reinforcer. In order to evaluate (a) reinforcer enhancement by nicotine and (b) reinforcer devaluation in the absence of nicotine, all rats experienced two PR schedule sessions per day for 10 days. Experiment 3 involved nicotine (0.3 mg/kg) and a visual stimulus in place of sucrose reinforcement. In Experiment 4, rats received nicotine (0.3 mg/kg) either before or after a single PR schedule session for 10 days.
resultsExperiments 1 and 2 demonstrate that reinforcer devaluation is related to the occupation of nicotinic-acetylcholine receptors. Results from Experiment 3 provide some evidence that devaluation occurs with either sucrose or visual-stimulus reinforcement. Experiment 4 demonstrates that a necessary condition for reinforcer devaluation to occur is the concurrent exposure to the reinforcer and nicotine.
conclusionsReinforcer devaluation in rats emerges rapidly in a progressive, orderly fashion that coincides with accumulated exposure to nicotine. These results suggest that reinforcer devaluation may be a feature of nicotine that contributes to the abuse liability of tobacco products.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.