Cited by 232Nicotinic Acetylcholine Receptors StudySmoking Behavior and CessationNeuroscience and Neuropharmacology Research

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Regulation of Nicotinic Acetylcholine Receptor Numbers and Function by Chronic Nicotine Exposure

Gentry, C., Lukas, R.·2002·Current Drug Target -CNS & Neurological Disorders

DOI 10.2174/1568007023339184

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Abstract

Recent advances concerning effects of chronic nicotine exposure on nicotinic acetylcholine receptor (nAChR) expression are reviewed. Implications are assessed of these findings for roles of nAChR in health and disease and for design of drugs for treatment of neurological and psychiatric disorders. Most studies continue to show that chronic nicotine exposure induces increases in numbers of nAChR-like binding or antigenic sites ("upregulation") across all nAChR subtypes investigated, but with time- and dose-dependencies and magnitudes for these effects that are unique to subsets of nAChR subtypes. These effects appear to be post-transcriptionally based, but mechanisms involved remain obscure. With notable exceptions, most studies also show that chronic nicotine exposure induces several phases of nAChR functional loss ("desensitization" and longer-lasting "persistent inactivation") assessed in response to acute nicotinic agonist challenges. Times for onset and recovery and dose-dependencies for nicotine-induced functional loss also are nAChR subtype-specific. Some findings suggest that upregulation and functional loss are not causally- or mechanistically-related. It is suggested that upregulation is not as physiologically significant in vivo as functional effects of chronic nicotine exposure. By contrast, brain levels of nicotine in tobacco users, and perhaps levels of acetylcholine in the extracellular space, clearly are in the range that would alter the balance between nAChR in functionally ready or inactivated states. Further work is warranted to illuminate how effects of chronic nicotinic ligand exposure are integrated across nAChR subtypes and the neuronal circuits and chemical signaling pathways that they service to produce nicotine dependence and/or therapeutic benefit.

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Authors: Gentry, C., & Lukas, R.
Affiliations: Barrow Neurological Institute (US)
Venue: Current Drug Target -CNS & Neurological Disorders
Publisher: Bentham Science Publishers Ltd.
Published: 2002-08-01
Volume: 1
Issue: 4
Pages: 359-385
ISSN: 1568-007X (ISSN-L)
DOI: 10.2174/1568007023339184
OpenAlex: W2024690874
Cited by: 232
References: 0
Citations by year: 2026: 1 · 2025: 4 · 2024: 4 · 2023: 2 · 2022: 2 · 2021: 4 · 2020: 25 · 2019: 3 · 2018: 4 · 2017: 5 · 2016: 14 · 2015: 5 · 2014: 8 · 2013: 12 · 2012: 7
FWCI: 2.99
Type: journal article
Language: en
Open access: closed
Locations: CNS & Neurological Disorders - Drug Targets (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Smoking Behavior and Cessation
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords: nicotinic acetylcholine receptors, chronic nicotine exposure, receptor up-regulation, receptor desensitization, nAChR subtypes, post-transcriptional regulation, nicotine dependence, acetylcholine, tobacco use, nicotinic agonists
MeSH terms: Animals, Humans, Ligands, Nicotine, Receptors, Nicotinic, Tobacco Use Disorder, Up-Regulation, Nicotinic Agonists

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Regulation of Nicotinic Acetylcholine Receptor Numbers and Function by Chronic Nicotine Exposure

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