Nicotine dependence produces hyperalgesia: Role of corticotropin-releasing factor-1 receptors (CRF1Rs) in the central amygdala (CeA)
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Because tobacco use has a large negative health and financial impact on society, it is critical to identify the factors that drive excessive use. These factors include the aversive withdrawal symptoms that manifest upon cessation of tobacco use, and may include increases in nociceptive processing. Corticotropin-releasing factor (CRF) signalling in the central amygdala (CeA) has been attributed an important role in: (1) central processing of pain, (2) excessive nicotine use that results in nicotine dependence, and (3) in mediating the aversive symptoms that manifest following cessation of tobacco exposure. Here, we describe three experiments in which the main hypothesis was that CRF/CRF1 receptor (CRF1R) signalling in the CeA mediates nicotine withdrawal-induced increases in nociceptive sensitivity in rats that are dependent on nicotine. In Experiment 1, nicotine-dependent rats withdrawn from chronic intermittent (14-h/day) nicotine vapor exhibited decreased hind paw withdrawal latencies in response to a painful thermal stimulus in the Hargreaves test, and this effect was attenuated by systemic administration of the CRF1R antagonist, R121919. In Experiment 2, nicotine-dependent rats withdrawn from nicotine vapor exhibited robust increases in mRNA for CRF and CRF1Rs in CeA. In Experiment 3, intra-CeA administration of R121919 reduced thermal nociception only in nicotine-dependent rats. Collectively, these results suggest that nicotine dependence increases CRF/CRF1R signalling in the CeA that mediates withdrawal-induced increases in sensitivity to a painful stimulus. Future studies will build on these findings by exploring the hypothesis that nicotine withdrawal-induced reduction in pain thresholds drive excessive nicotine use via CRF/CRF1R signalling pathways.
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CRF/CRF1 receptor signaling in the CeA mediates nicotine withdrawal-induced increases in nociceptive sensitivity in nicotine-dependent rats.
“The CRF/CRF1 receptor signaling in the CeA also mediates nicotine withdrawal-induced increases in nociceptive sensitivity in rats that are dependent on nicotine (Baiamonte et al. 2014).”
From Nicotine Withdrawal (2015) · cites this paper as Baiamonte et al. 2014
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- Authors
- Baiamonte, B. A., Valenza, M., Roltsch, E. A., Whitaker, A. M., Baynes, B. B., Sabino, V., & Gilpin, N. W.
- Affiliations
- Louisiana State University Health Sciences Center New Orleans (US)
- Boston University (US)
- Corresponding author
- Gilpin, Nicholas W.
- Venue
- Neuropharmacology
- Publisher
- Elsevier BV
- Published
- 2014-02
- Volume
- 77
- Pages
- 217-223
- ISSN
- 0028-3908 (ISSN-L)
- PMC
- PMC4144034
- OpenAlex
- W2021284157
- Cited by
- 58
- References
- 75
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 3 · 2023: 6 · 2022: 4 · 2021: 4 · 2020: 10 · 2019: 6 · 2018: 5 · 2017: 2 · 2016: 4 · 2015: 5 · 2014: 3
- FWCI
- 2.78
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neuropharmacology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- IRIS Research product catalog (Sapienza University of Rome) (submittedVersion)
- Funders
- LSUHSC Start-Up funds (MH093650)
- NIH (AA016731)
- Topics
- Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
- Keywords
- nicotine dependence, hyperalgesia, corticotropin-releasing factor, CRF1 receptor, central amygdala, nicotine withdrawal, thermal nociception, tobacco use, pain sensitivity
- MeSH terms
- CRF Receptor, Type 1, Amygdala, Animals, Corticotropin-Releasing Hormone, Hyperalgesia, Male, Nicotine, Pyrimidines, Substance Withdrawal Syndrome, Tobacco Use Disorder, Rats, Wistar, Pain Threshold, Receptors, Corticotropin-Releasing Hormone, Rats
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