Cited by 187Nicotinic Acetylcholine Receptors StudySmoking Behavior and CessationNeuroscience and Neuropharmacology Research

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Chronic Nicotine Treatment Up-regulates Human α3β2 but Not α3β4 Acetylcholine Receptors Stably Transfected in Human Embryonic Kidney Cells

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Wang, Fan, Nelson, Mark E., Kuryatov, Alexander, Olale, Felix, Cooper, John, Keyser, Kent, Lindstrom, Jon·1998·Journal of Biological Chemistry

DOI 10.1074/jbc.273.44.28721

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Abstract

Human nicotinic acetylcholine receptor (AChR) subtypes alpha3 beta2, alpha3 beta2 alpha5, alpha3 beta4, and alpha3 beta4 alpha5 were stably expressed in cells derived from the human embryonic kidney cell line 293. alpha3 beta4 AChRs were found in prominent 2-micrometer patches on the cell surface, whereas most alpha3 beta2 AChRs were more diffusely distributed. The functional properties of the alpha3 AChRs in tsA201 cells were characterized by whole cell patch clamp using both acetylcholine and nicotine as agonists. Nicotine was a partial agonist on alpha3 beta4 AChRs and nearly a full agonist on alpha3 beta2 alpha5 AChRs. Chronic exposure of cells expressing alpha3 beta2 AChRs or alpha3 beta2 alpha5 AChRs to nicotine or carbamylcholine increased their amount up to 24-fold but had no effect on the amount of alpha3beta4 or alpha3 beta4 alpha5 AChRs, i.e. the up-regulation of alpha3 AChRs depended on the presence of beta2 but not beta4 subunits in the AChRs. This was also found to be true of alpha3 AChRs in the human neuroblastoma SH-SY5Y. In the absence of nicotine, alpha3 beta2 AChRs were expressed at much lower levels than alpha3 beta4 AChRs, but in the presence of nicotine, the amount of alpha3 beta2 AChRs exceeded that of alpha3 beta4 AChRs. Up-regulation was seen for both total AChRs and surface AChRs. Up-regulated alpha3beta2 AChRs were functional. The nicotinic antagonists curare and dihydro-beta-erythroidine also up-regulated alpha3 beta2 AChRs, but only by 3-5-fold. The channel blocker mecamylamine did not cause up-regulation of alpha3 beta2 AChRs and inhibited up-regulation by nicotine. Our data suggest that up-regulation of alpha3 beta2 AChRs in these lines by nicotine results from both increased subunit assembly and decreased AChR turnover.

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Authors: Wang, F., Nelson, M. E., Kuryatov, A., Olale, F., Cooper, J., Keyser, K., & Lindstrom, J.
Affiliations: University of Pennsylvania (US)
University of Alabama at Birmingham (US)
Corresponding author: Lindstrom, Jon
ORCID: Nelson, Mark E.
Venue: Journal of Biological Chemistry
Publisher: Elsevier BV
Published: 1998-11
Volume: 273
Issue: 44
Pages: 28721-28732
ISSN: 0021-9258 (ISSN-L)
DOI: 10.1074/jbc.273.44.28721
OpenAlex: W2052494845
Cited by: 187
References: 56
Citations by year: 2025: 1 · 2024: 1 · 2023: 3 · 2022: 1 · 2021: 1 · 2020: 4 · 2019: 4 · 2018: 2 · 2017: 2 · 2016: 3 · 2015: 12 · 2014: 4 · 2013: 6 · 2012: 1
FWCI: 4.19
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
creativecommons.org/licenses/by/4.0/ (vor, 8004 d)
Locations: Journal of Biological Chemistry (publishedVersion, cc-by)
PubMed (publishedVersion)
Funders: National Institute of Neurological Disorders and Stroke (NS11323, F32NS010333, R01NS011323, NS10333)
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, receptor up-regulation, chronic nicotine exposure, receptor subunit assembly, receptor turnover, partial agonism, nicotinic antagonists, mecamylamine, curare, dihydro-beta-erythroidine, SH-SY5Y cells, tsA201 cells
MeSH terms: Animals, Cell Line, Humans, Mecamylamine, Nicotine, Receptors, Cholinergic, Transfection, Xenopus laevis, Up-Regulation, Cholinergic Agonists, Cholinergic Antagonists

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Chronic Nicotine Treatment Up-regulates Human α3β2 but Not α3β4 Acetylcholine Receptors Stably Transfected in Human Embryonic Kidney Cells

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