ArticleBiological psychiatry2009
Corticotropin-releasing factor-1 receptor activation mediates nicotine withdrawal-induced deficit in brain reward function and stress-induced relapse.
Article in Biological psychiatry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 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
84 citing papers in PubMed, 132 citations in OpenAlex.
- The influence of stress and social defeat on neurobiological reinforcement mechanisms across reward to withdrawal in nicotine addiction.Psychopharmacology · 2025Review
- Neurobiology of Stress-Induced Nicotine Relapse.International journal of molecular sciences · 2024Review
- Chronic Nicotine Consumption and Withdrawal Regulate Melanocortin Receptor, CRF, and CRF Receptor mRNA Levels in the Rat Brain.Brain sciences · 2024Article
- Sex differences in nicotine intake and relapse behavior in nicotine-dependent adult wistar rats.Frontiers in pharmacology · 2024Article
- Development of Dependence in Smokers and Rodents With Voluntary Nicotine Intake: Similarities and Differences.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2023Review
- The D1/D2-like receptor antagonist flupentixol and the D2-like receptor antagonist L-741626 decrease operant responding for nicotine and food and locomotor activity in male and female rats.Journal of psychopharmacology (Oxford, England) · 2023Article
- Corticotropin releasing factor and drug seeking in substance use disorders: Preclinical evidence and translational limitations.Addiction neuroscience · 2022Article
- Actions of feeding-related peptides on the mesolimbic dopamine system in regulation of natural and drug rewards.Addiction neuroscience · 2022Article
- Rewarding Effects of Nicotine Self-administration Increase Over Time in Male and Female Rats.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2021Article
- Converging vulnerability factors for compulsive food and drug use.Neuropharmacology · 2021Review
- The Role of the Central Amygdala in Alcohol Dependence.Cold Spring Harbor perspectives in medicine · 2021Review
- Drug addiction co-morbidity with alcohol: Neurobiological insights.International review of neurobiology · 2021Review
- Adolescent nicotine and tobacco smoke exposure enhances nicotine self-administration in female rats.Neuropharmacology · 2020Article
- Role of corticotropin-releasing factor in alcohol and nicotine addiction.Brain research · 2020Review
- Evaluation of Sex Differences in the Elasticity of Demand for Nicotine and Food in Rats.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2020Article
- Rewarding Effects of Nicotine in Adolescent and Adult Male and Female Rats as Measured Using Intracranial Self-stimulation.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2020Article
- Overexpression of corticotropin-releasing factor in the nucleus accumbens enhances the reinforcing effects of nicotine in intact female versus male and ovariectomized female rats.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020Article
- Sex differences in the reward deficit and somatic signs associated with precipitated nicotine withdrawal in rats.Neuropharmacology · 2019Article
- Neurobiological and Neurophysiological Mechanisms Underlying Nicotine Seeking and Smoking Relapse.Molecular neuropsychiatry · 2019Review
- Deletion of CRH From GABAergic Forebrain Neurons Promotes Stress Resilience and Dampens Stress-Induced Changes in Neuronal Activity.Frontiers in neuroscience · 2019Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundTobacco addiction is a chronic brain disorder that is characterized by a negative affective state upon smoking cessation and relapse after periods of abstinence. Previous research has shown that blockade of corticotropin-releasing factor (CRF) receptors with a nonspecific CRF1/CRF2 receptor antagonist prevents the deficit in brain reward function associated with nicotine withdrawal and stress-induced reinstatement of extinguished nicotine-seeking in rats. The aim of these studies was to investigate the role of CRF1 and CRF2 receptors in the deficit in brain reward function associated with precipitated nicotine withdrawal and stress-induced reinstatement of nicotine-seeking.
methodsThe intracranial self-stimulation (ICSS) procedure was used to assess the negative affective state of nicotine withdrawal. Elevations in brain reward thresholds are indicative of a deficit in brain reward function. Stress-induced reinstatement of nicotine-seeking was investigated in animals in which responding for intravenously infused nicotine was extinguished by substituting saline for nicotine.
resultsIn the ICSS experiments, the nicotinic receptor antagonist mecamylamine elevated the brain reward thresholds of the nicotine-dependent rats but not those of the control rats. The CRF1 receptor antagonist R278995/CRA0450 but not the CRF2 receptor antagonist astressin-2B prevented the elevations in brain reward thresholds associated with precipitated nicotine withdrawal. Furthermore, R278995/CRA0450 but not astressin-2B prevented stress-induced reinstatement of extinguished nicotine-seeking. Neither R278995/CRA0450 nor astressin-2B affected operant responding for chocolate-flavored food pellets.
conclusionsThese studies indicate that CRF(1) receptors but not CRF(2) receptors play an important role in the anhedonic-state associated with acute nicotine withdrawal and stress-induced reinstatement of nicotine-seeking.
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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.