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Regulation of Nicotinic Acetylcholine Receptor Numbers and Function by Chronic Nicotine Exposure
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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In the citing paper
“A number of studies have shown that chronic administration of nicotinic agonists (including nicotine through regular smoking or as delivered through the nicotine patch) can desensitize rather than activate nAChRs (Reitstetter et al., 1999), leading to functional antagonism (Gentry and Lukas, 2002; Quick and Lester, 2002).”
From It is not “either/or”: Activation and desensitization of nicotinic acetylcholine receptors both contribute to behaviors related to nicotine addiction and mood (2008) · cites this paper as Gentry and Lukas, 2002
In the citing paper
“In fact, nAChRs recover from desensitization on the scale of seconds to hours (Gentry and Lukas 2002).”
From Nicotine Withdrawal (2015) · cites this paper as Gentry and Lukas 2002
In the citing paper
“Relevant to the understanding of the neuroadaptations produced by nicotine is the fact that nAChR upregulation differs among receptor subtypes, varies among brain regions for the same subtype, and even depends on the contingency of nicotine administration [9, 90, 93].”
From Mechanistic insights into nicotine withdrawal (2011) · cites this paper as [93]
In the citing paper
“Chronic nicotine treatment results in an upregulation of β2* nAChRs (Marks et al., 1983; Schwartz and Kellar, 1983) but also a desensitization of nAChRs (Gentry and Lukas, 2002).”
From The duration of nicotine withdrawal-associated deficits in contextual fear conditioning parallels changes in hippocampal high affinity nicotinic acetylcholine receptor upregulation (2012) · cites this paper as Gentry and Lukas, 2002
In the citing paper
“in vitro studies have shown that nAChRs return from a desensitized state in minutes to hours (see Gentry and Lukas (2002) for review).”
From The duration of nicotine withdrawal-associated deficits in contextual fear conditioning parallels changes in hippocampal high affinity nicotinic acetylcholine receptor upregulation (2012) · cites this paper as Gentry and Lukas (2002)
In the citing paper
“But increasing evidence suggests that upregulation of high-sensitivity nAChRs is, at least partially, the basis for several key biological results of chronic nicotine administration: tolerance, locomotor sensitization, and cognitive sensitization (5,10–12).”
From Nicotine is a selective pharmacological chaperone of acetylcholine receptor number and stoichiometry. Implications for drug discovery (2009) · cites this paper as [11]
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Metadata
- 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)
- 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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