CRF–CRF 1 system activation mediates withdrawal-induced increases in nicotine self-administration in nicotine-dependent rats
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Nicotine, the main psychoactive ingredient of tobacco, induces negative emotional symptoms during abstinence that contribute to a profound craving for nicotine. However, the neurobiological mechanisms underlying how nicotine produces dependence remains poorly understood. We demonstrate one mechanism for both the anxiety-like symptoms of withdrawal and excessive nicotine intake observed after abstinence, through recruitment of the extrahypothalamic stress peptide corticotropin-releasing factor (CRF) system and activation of CRF 1 receptors. Overactivation of the CRF–CRF 1 system may contribute to nicotine dependence and may represent a prominent target for investigating the vulnerability to tobacco addiction.
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Nicotine withdrawal increases CRF in the CeA, and blockade of CRF1 receptors reduces nicotine withdrawal-induced anxiety-like behavior.
“Nicotine withdrawal leads to an increase in CRF in the CeA, and blockade of CRF1 receptors diminishes nicotine withdrawalinduced anxiety-like behavior (George et al. 2007).”
From Nicotine Withdrawal (2015) · cites this paper as George et al. 2007
CRF levels increase by more than 500% in the CeA after mecamylamine-precipitated nicotine withdrawal.
“CRF levels increase by >500% in the CeA after nicotine withdrawal is precipitated with the nAChR antagonist mecamylamine [158].”
From Mechanistic insights into nicotine withdrawal (2011) · cites this paper as [158]
Injection of a CRF1 receptor antagonist into the CeA blunts anxiety-like behavior during nicotine withdrawal.
“Injection of a CRF1 receptor antagonist into the CeA blunts anxiety-like behavior during nicotine withdrawal [158].”
From Mechanistic insights into nicotine withdrawal (2011) · cites this paper as [158]
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- Authors
- George, O., Ghozland, S., Azar, M. R., Cottone, P., Zorrilla, E. P., Parsons, L. H., O'Dell, L. E., Richardson, H. N., & Koob, G. F.
- Affiliations
- Scripps Research Institute (US)
- Department of Psychology, University of Texas, El Paso, TX 79968
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2007-10-23
- Volume
- 104
- Issue
- 43
- Pages
- 17198-17203
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC2040467
- OpenAlex
- W2097077325
- Cited by
- 245
- References
- 45
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 7 · 2023: 9 · 2022: 4 · 2021: 11 · 2020: 9 · 2019: 17 · 2018: 17 · 2017: 11 · 2016: 14 · 2015: 14 · 2014: 16 · 2013: 22 · 2012: 16
- FWCI
- 12.46
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Robert Wood Johnson Foundation
- Tobacco-Related Disease Research Program (12RT-0099)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK 26741, P01DK026741)
- Topics
- Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Keywords
- nicotine dependence, nicotine self-administration, nicotine withdrawal, corticotropin-releasing factor, CRF1 receptor, anxiety-like behavior, tobacco dependence, nicotine craving
- MeSH terms
- CRF Receptor, Type 1, Amygdala, Animals, Anxiety, Behavior, Animal, Corticotropin-Releasing Hormone, Feeding Behavior, Male, Mecamylamine, Nicotine, Self Administration, Substance Withdrawal Syndrome, Behavior, Addictive, Rats, Wistar, Receptors, Corticotropin-Releasing Hormone, Rats
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