Cited by 456Nicotinic Acetylcholine Receptors StudyNeuroscience and Neuropharmacology ResearchReceptor Mechanisms and Signaling

Desensitization of neuronal nicotinic receptors

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Quick, Michael W., Lester, Robin A.J.·2002·Journal of Neurobiology

Abstract

The loss of functional response upon continuous or repeated exposure to agonist, desensitization , is an intriguing phenomenon if not as yet a well‐defined physiological mechanism. However, detailed evaluation of the properties of desensitization, especially for the superfamily of ligand‐gated ion channels, reveals how the nervous system could make important use of this process that goes far beyond simply curtailing excessive receptor stimulation and the prevention of excitotoxicity. Here we will review the mechanistic basis of desensitization and discuss how the subunit‐dependent properties and regulation of nicotinic acetylcholine receptor (nAChR) desensitization contribute to the functional diversity of these channels. These studies provide the essential framework for understanding how the physiological regulation of desensitization could be a major determinant of synaptic efficacy by controlling, in both the short and long term, the number of functional receptors. This type of mechanism can be extended to explain how the continuous occupation of desensitized receptors during chronic nicotine exposure contributes to drug addiction, and highlights the potential significance of prolonged nAChR desensitization that would also occur as a result of extended acetylcholine lifetime during treatment of Alzheimer's disease with cholinesterase inhibitors. Thus, a clearer picture of the importance of nAChR desensitization in both normal information processing and in various diseased states is beginning to emerge. © 2002 Wiley Periodicals, Inc. J Neurobiol 53: 457–478, 2002

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  1. Clementi F, Fornasari D, Gotti C, editors. Neuronal nic- otinic receptors. Berlin: Springer, p 13-30.

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Authors
Quick, M. W., & Lester, R. A. J.
Affiliations
University of Alabama at Birmingham (US)
Corresponding author
Lester, Robin A.J.
Venue
Journal of Neurobiology
Publisher
Wiley
Published
2002-11-15
Volume
53
Issue
4
Pages
457-478
ISSN
  • 0022-3034 (ISSN-L)
  • 1097-4695
OpenAlex
W2061475648
Cited by
456
References
163
Citations by year
2026: 8 · 2025: 9 · 2024: 9 · 2023: 10 · 2022: 12 · 2021: 14 · 2020: 15 · 2019: 24 · 2018: 15 · 2017: 17 · 2016: 19 · 2015: 22 · 2014: 23 · 2013: 21 · 2012: 21
FWCI
1.43
Type
journal article
Language
en
Open access
Locations
  • Journal of Neurobiology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institute on Drug Abuse (DA-11940, R01DA011940)
  • National Institute of Neurological Disorders and Stroke (NS13669)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
Keywords
receptor desensitization, nicotinic acetylcholine receptors, ligand-gated ion channels, receptor subunit composition, synaptic efficacy, chronic nicotine exposure, nicotine dependence, cholinesterase inhibitors, Alzheimer's disease, acetylcholine, excitotoxicity
MeSH terms
Acetylcholine, Animals, Drug Tolerance, Humans, Ion Channels, Membrane Potentials, Nicotine, Receptors, Nicotinic

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