ArticlePsychopharmacology2016
N-acetylcysteine decreased nicotine reward-like properties and withdrawal in mice.
Article in Psychopharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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.
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Who cites it
11 citing papers in PubMed, 30 citations in OpenAlex.
- Glutamine synthetase in astrocytes of the caudate and putamen is responsible for locomotor sensitization after nicotine exposure.Acta pharmaceutica Sinica. B · 2025Article
- Selective Effects of Acutely Administered N-Acetyl-Cysteine in Rodent Models of Nicotine-Conditioned Behaviours.Addiction biology · 2025Article
- The potential effect of α7 nicotinic receptors modulation on palatable food-induced dependence-like behaviors.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2024Article
- N-acetylcysteine for smoking cessation among dual users of tobacco and cannabis: Protocol and rationale for a randomized controlled trial.Contemporary clinical trials · 2023Article
- The Potential of N-Acetyl-L-Cysteine (NAC) in the Treatment of Psychiatric Disorders.CNS drugs · 2022Review
- N-acetylcysteine in substance use disorder: a lesson from preclinical and clinical research.Pharmacological reports : PR · 2021Review
- Glial cells as therapeutic targets for smoking cessation.Neuropharmacology · 2020Review
- Review
- Behavioral effects of psychostimulants in mutant mice with cell-type specific deletion of CB2 cannabinoid receptors in dopamine neurons.Behavioural brain research · 2019Article
- Acquisition, Maintenance and Relapse-Like Alcohol Drinking: Lessons from the UChB Rat Line.Frontiers in behavioral neuroscience · 2017Review
- Disentangling the Role of Astrocytes in Alcohol Use Disorder.Alcoholism, clinical and experimental research · 2016Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
rationaleN-acetylcysteine can increase extrasynaptic glutamate and reduce nicotine self-administration in rats and smoking rates in humans.
objectivesThe aim of this study was to determine if N-acetylcysteine modulates the development of nicotine place conditioning and withdrawal in mice.
methodsN-acetylcysteine was given to nicotine-treated male ICR mice. Experiment 1: reward-like behavior. N-acetylcysteine (0, 5, 15, 30, or 60 mg/kg, i.p.) was given 15 min before nicotine (0.5 mg/kg, s.c.) or saline (10 ml/kg, s.c.) in an unbiased conditioned place preference (CPP) paradigm. Conditioning for highly palatable food served as control. Experiment 2: spontaneous withdrawal. The effect of N-acetylcysteine (0, 15, 30, 120 mg/kg, i.p.) on anxiety-like behavior, somatic signs, and hyperalgesia was measured 18-24 h after continuous nicotine (24 mg/kg/day, 14 days). Experiment 3: mecamylamine-precipitated, withdrawal-induced aversion. The effect of N-acetylcysteine (0, 15, 30, 120 mg/kg, i.p.) on mecamylamine (3.5 mg/kg, i.p.)-precipitated withdrawal was determined after continuous nicotine (24 mg/kg, i.p., 28 days) using the conditioned place aversion (CPA) paradigm.
resultsDose-related reductions in the development of nicotine CPP, somatic withdrawal signs, hyperalgesia, and CPA were observed after N-acetylcysteine pretreatment. No effect of N-acetylcysteine was found on palatable food CPP, anxiety-like behavior, or motoric capacity (crosses between plus maze arms). Finally, N-acetylcysteine did not affect any measure in saline-treated mice at doses effective in nicotine-treated mice.
conclusionsThese are the first data suggesting that N-acetylcysteine blocks specific mouse behaviors associated with nicotine reward and withdrawal, which adds to the growing appreciation that N-acetylcysteine may have high clinical utility in combating nicotine dependence.
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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.