CoChat
Sign Up
Cited by 65Nicotinic Acetylcholine Receptors StudySmoking Behavior and CessationNeuroscience and Neuropharmacology Research

Up-regulation of nicotinic acetylcholine receptors following chronic exposure of rats to mainstream cigarette smoke or α4β2 receptors to nicotine

Yates, Stephen L., Bencheri, Merouane, Fluhler, Eric N., Lippiello, Patrick M.·1995·Biochemical Pharmacology
DOI 10.1016/0006-2952(95)02100-0
Open this paper in CoChat — free account

Abstract

Smokers are reported to have a higher density of central nicotinic acetylcholine receptors (nAChRs) that non-smokers at autopsy. Whether this increased receptor density is a response to smoking or a result of genetic variability is not known. While sub-chronic treatment of rats and mice with nicotine results in upregulation of central nAChRs, changes in receptor density in response to cigarette smoke have not been studied previously. In this study, male Sprague-Dawley rats were exposed nose-only for 13 weeks to mainstream cigarette smoke followed by assessment of [3H]nicotine binding in five brain regions of smoke- and sham-exposed animals. In smoke-exposed animals, there was a significant increase in nAChR density in the cortex, striatum, and cerebellum (35, 25, and 31% increases, respectively), while there was no significant change in receptor density in the thalamus and hippocampus. Smoke exposure did not alter markedly the affinity of the receptor for nicotine in these brain regions. Furthermore, up-regulation of nAChRs did not alter the biphasic binding properties by which nicotine binds to its receptor. There were no changes in the association (fast phase) or isomerization (slow phase) rate constants, and the percent contribution of slow and fast phase binding to nAChRs was not altered in the up-regulated receptor population compared with control. Similar results were observed following chronic nicotine exposure of cultured cortical cells from fetal rat brain or cells transfected with the alpha 4 beta 2 nAChR subtype. These results show that the up-regulation following smoke exposure in the rat is phenomenologically similar to that observed in vitro. These data provide preliminary evidence for a relationship between cigarette smoking and nAChR up-regulation in vivo and suggest that similar mechanisms of upregulation may underlie chronic smoke exposure of live animals and nicotine exposure of artificially expressed alpha 4 beta 2 receptors in vitro.

Integrity signals

Registry

Crossref · 10.1016/0006-2952(95)02100-0

Cites

41 of 41 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Evidence indicates that α4β2* nAChRs do not down-regulate in response to lasting cholinergic stimulation.

    “Evidence indicating that α4β2* nAChRs do not down-regulate in response to lasting cholinergic stimulation (Walsh et al, 2008, Yates et al, 1995) is consistent with this assumption.”

    From Modes and models of forebrain cholinergic neuromodulation of cognition (2011) · cites this paper as Yates et al, 1995

Cites

Flagged first, then by citations

3 of the 44 references couldn’t be matched to a known paper.

Cited by

Sorted by citations

Related

Authors
Yates, S. L., Bencheri, M., Fluhler, E. N., & Lippiello, P. M.
Affiliations
  • Duke University (US)
  • Reynolds American (United States) (US)
Venue
Biochemical Pharmacology
Publisher
Elsevier BV
Published
1995-12
Volume
50
Issue
12
Pages
2001-2008
ISSN
0006-2952 (ISSN-L)
DOI
10.1016/0006-2952(95)02100-0
OpenAlex
W2091661891
Cited by
65
References
44
Citations by year
2022: 2 · 2021: 1 · 2020: 5 · 2019: 2 · 2018: 3 · 2016: 4 · 2015: 2 · 2014: 1 · 2013: 5 · 2012: 5
FWCI
0.50
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Biochemical Pharmacology (publishedVersion)
  • PubMed (publishedVersion)
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
nicotinic acetylcholine receptors, receptor up-regulation, cigarette smoke exposure, alpha4beta2 nicotinic receptor, nicotine, receptor density, cortical cells, brain regions, smoking
MeSH terms
Animals, Binding Sites, Brain, Cell Line, Kinetics, Male, Nicotine, Receptors, Nicotinic, Smoking, Up-Regulation, Rats, Sprague-Dawley, Mice, Rats

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review