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Cited by 112Nicotinic Acetylcholine Receptors StudySmoking Behavior and CessationNeuroscience and Neuropharmacology Research

Long-Term Nicotine Treatment Decreases Striatal α6* Nicotinic Acetylcholine Receptor Sites and Function in Mice

Lai, Albert, Parameswaran, Neeraja, Khwaja, Mirium, Whiteaker, Paul, Lindstrom, Jon M., Fan, Hong, McIntosh, J. Michael, Grady, Sharon R. +1 more·2005·Molecular Pharmacology
DOI 10.1124/mol.104.006429
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Abstract

Alpha-conotoxin MII-sensitive nicotinic acetylcholine receptors (nAChRs) are distinct from other subtypes in their relatively restricted localization to the striatum and some other brain regions. The effect of nicotine treatment on nAChR subtypes has been extensively investigated, with the exception of changes in alpha-conotoxin MII-sensitive receptor expression. We therefore determined the consequence of long-term nicotine administration on this subtype and its function. Nicotine was given in drinking water to provide a long-term yet intermittent treatment. Consistent with previous studies, nicotine exposure increased 125I-epibatidine and 125I-A85380 (3-[2-(S)-azetidinylmethoxy]pyridine), but not 125I-alpha-bungarotoxin, receptors in cortex and striatum. We observed an unexpected reduction (30%) in striatal 125I-alpha-conotoxin MII sites, which occurred because of a decrease in B(max). This decline was more robust in older (>8-month-old) compared with younger (2-4-month-old) mice, suggesting age is important for nicotine-induced disruption of nAChR phenotype. Immunoprecipitation experiments using nAChR subunit-directed antibodies indicate that alterations in subunit-immunoreactivity with nicotine treatment agree with those in the receptor binding studies. To determine the relationship between striatal nAChR sites and function, we measured nicotine-evoked [3H]dopamine release. A decline was obtained with nicotine treatment that was caused by a selective decrease in alpha-cono…

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Crossref · 10.1124/mol.104.006429

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  • Different β2*-subunit combinations appear to be differentially regulated by nicotine, with α3/α6 and α6α4β2* and α5α4β2* not upregulating or decreasing in response to nicotine while α6β2 (nonα4) nAChR increase in response to nicotine.

    “Importantly, different β2*-subunit combinations appear to be differentially regulated by nicotine, with α3/α6 and α6α4β2* and α5α4β2* not upregulating or decreasing in response to nicotine38, 85-88 while α6β2 (nonα4) nAChR increase in response to nicotine88.”

    From β2-Nicotinic Acetylcholine Receptor Availability During Acute and Prolonged Abstinence From Tobacco Smoking (2009) · cites this paper as [85]

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Authors
Lai, A., Parameswaran, N., Khwaja, M., Whiteaker, P., Lindstrom, J. M., Fan, H., McIntosh, J. M., Grady, S. R., & Quik, M.
Affiliations
  • Parkinson's Institute and Clinical Center (US)
  • University of Colorado Boulder (US)
  • University of Pennsylvania (US)
  • Johns Hopkins University (US)
ORCID
Venue
Molecular Pharmacology
Publisher
Elsevier BV
Published
2005-05
Volume
67
Issue
5
Pages
1639-1647
ISSN
0026-895X (ISSN-L)
DOI
10.1124/mol.104.006429
OpenAlex
W1981632227
Cited by
112
References
12
Citations by year
2025: 1 · 2024: 1 · 2023: 8 · 2022: 1 · 2021: 3 · 2020: 4 · 2019: 2 · 2018: 1 · 2016: 4 · 2015: 9 · 2014: 6 · 2013: 8 · 2012: 6
FWCI
3.76
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Molecular Pharmacology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institute of Mental Health (MH53631)
  • National Institute on Drug Abuse (R01DA012242, DA12242)
  • National Institute of Neurological Disorders and Stroke (R01NS047162, NS42091, NS47162, NS1323, R01NS042091)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
  • Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords
striatum, receptor down-regulation, dopamine release, receptor subunit composition, age-dependent effects, alpha4 nAChR, alpha-bungarotoxin binding, epibatidine binding
MeSH terms
Animals, Corpus Striatum, Dose-Response Relationship, Drug, Male, Mice, Inbred C57BL, Nicotine, Protein Binding, Receptors, Nicotinic, Time Factors, Mice

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