ArticlePsychopharmacology2006
beta2-Subunit-containing nicotinic acetylcholine receptors are involved in nicotine-induced increases in conditioned reinforcement but not progressive ratio responding for food in C57BL/6 mice.
Article in Psychopharmacology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 70 citations in OpenAlex.
- Nicotinic acetylcholine receptor beta2 subunit gene implicated in a systems-based candidate gene study of smoking cessation.Human molecular genetics · 2008Trial
- Elucidating the reinforcing effects of nicotine: a tribute to Nadia Chaudhri.Psychopharmacology · 2023Review
- Midazolam, methamphetamine, morphine and nicotine intake in high-drinking-in-the-dark mice.Addiction biology · 2022Article
- β2* nicotinic acetylcholine receptor subtypes mediate nicotine-induced enhancement of Pavlovian conditioned responding to an alcohol cue.Frontiers in behavioral neuroscience · 2022Article
- Mechanisms of Nicotine Addiction.Cold Spring Harbor perspectives in medicine · 2021Review
- Partial and full deletion of nicotinic acetylcholine receptor α4 and β2 subunits reduces sensitivity to acute nicotine administration and development of tolerance following chronic nicotine administration.Behavioural pharmacology · 2020Article
- Developmental nicotine exposure engenders intergenerational downregulation and aberrant posttranslational modification of cardinal epigenetic factors in the frontal cortices, striata, and hippocampi of adolescent mice.Epigenetics & chromatin · 2020Article
- Nicotinic Acetylcholine Receptor Signaling in the Hypothalamus: Mechanisms Related to Nicotine's Effects on Food Intake.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2020Review
- Nicotine Self-Administration With Tobacco Flavor Additives in Male Rats.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2020Article
- Developmental nicotine exposure elicits multigenerational disequilibria in proBDNF proteolysis and glucocorticoid signaling in the frontal cortices, striata, and hippocampi of adolescent mice.Biochemical pharmacology · 2019Article
- Adolescent and adult nicotine exposure differentially impacts oral nicotine and oral saccharin self-administration in mice.Behavioural brain research · 2019Article
- Effects of nicotine on homeostatic and hedonic components of food intake.The Journal of endocrinology · 2017Review
- Oral operant ethanol self-administration in the absence of explicit cues, food restriction, water restriction and ethanol fading in C57BL/6J mice.Psychopharmacology · 2015Article
- Muscarinic, but not nicotinic, acetylcholine receptor blockade in the ventral tegmental area attenuates cue-induced sucrose-seeking.Behavioural brain research · 2015Article
- Inside-out neuropharmacology of nicotinic drugs.Neuropharmacology · 2015Review
- Distinct effects of ventral tegmental area NMDA and acetylcholine receptor blockade on conditioned reinforcement produced by food-associated cues.Neuroscience · 2015Article
- Nicotinic receptor contributions to smoking: insights from human studies and animal models.Current addiction reports · 2015Article
- Responding for conditioned reinforcement in C57BL/6 and CD-1 mice, and Sprague-Dawley rats: Effects of methylphenidate and amphetamine.Psychopharmacology · 2014Article
- Repeated nicotine exposure during adolescence alters reward-related learning in male and female rats.Behavioural brain research · 2014Article
- Molecules and circuits involved in nicotine addiction: The many faces of smoking.Neuropharmacology · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
rationaleNicotine administration potentiates conditioned reinforcement in rats, an effect that persists for weeks after chronic exposure. Little is known regarding the nicotinic receptor subtypes that may mediate this effect.
objectiveThe purpose of this study was to determine whether beta2-subunit-containing nicotinic acetylcholine receptors (beta2*nAChRs) are necessary for lasting effects of nicotine on conditioned and primary reinforcement in mice.
methodsBeta2 knockout (beta2KO) and wild-type (WT) mice received 14 days of nicotine exposure (NIC, 200 microg/ml in 2% saccharin) or saccharin alone (SAC) in their drinking water. Five days later, mice received paired presentations of a conditioned stimulus (CS) with water unconditioned stimulus (US) or explicitly unpaired presentations of the CS and US during Pavlovian discriminative approach training. Training was followed by two conditioned reinforcement tests. Mice were subsequently tested for food-reinforced responding in the absence of explicit cues followed by a progressive ratio test.
resultsDuring conditioned reinforcement testing, only mice in the paired condition showed increased responding in the CS-reinforced aperture over inactive apertures. WT-NIC mice showed enhanced conditioned reinforcement compared to WT-SAC animals. beta2KO-SAC mice showed elevated conditioned reinforcement compared to WT-SAC subjects, but beta2KO-NIC and beta2KO-SAC mice did not differ in responding with conditioned reinforcement. Prior nicotine exposure did not alter food-reinforced responding but resulted in elevated break points for food in both genotypes.
conclusionThese data show that nicotine exposure enhances conditioned reinforcement in mice and indicate that beta2*nAChRs are necessary for nicotine-dependent enhancement of incentive aspects of motivation but not motivation for primary reinforcement measured by progressive ratio responding.
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.