Effect of smoking history on [3H]nicotine binding in human postmortem brain
Abstract
Chronic nicotine administration in animal models evokes a dose-dependent increase in brain nicotinic receptor numbers. Genetically determined variability in nicotinic receptor number in different mouse strains has also been reported, which is thought to affect sensitivity to nicotine, as well as the development of tolerance. Humans self-administer nicotine principally in the form of cigarettes and other tobacco products. The present study compared [3H]nicotine binding in human postmortem brain from thalamus and hippocampus of nonsmoking subjects, subjects who had variable life-long smoking histories and subjects who had quit smoking. A significant increase was seen in [3H]nicotine binding in both hippocampus and thalamus of subjects with life-long smoking histories. In the hippocampus, this change resulted from a change in total receptor number (Bmax), with no change in receptor affinity (Kd). There was also a positive correlation between the degree of smoking, as measured by the average reported packs smoked per day, and the number of nicotine binding sites found in both the hippocampus and thalamus, showing that humans exhibit a dose-dependent increase in brain nicotinic receptor binding. Receptor levels in these brain regions after smoking cessation were at or below those found in the control population, which indicated that smoking-induced changes are reversible after cessation of nicotine treatment. These results suggest that increases in nicotinic receptor levels in the human brain may underlie nicotine tolerance and addiction in smokers.
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A postmortem human study indicated that individuals who had quit smoking at least 2 months prior to their death had nicotine binding levels similar to control nonsmokers.
“A postmortem human study indicated that individuals who had quit smoking at least 2 months prior to their death (range 2 months-30 years) had nicotine binding levels similar to control nonsmokers2.”
From β2-Nicotinic Acetylcholine Receptor Availability During Acute and Prolonged Abstinence From Tobacco Smoking (2009) · cites this paper as [2]
This study and previous in vivo PET and SPECT studies report no upregulation of thalamic β2*-nAChR availability during acute abstinence.
“This study and previous in vivo PET78 and SPECT8, 18 studies report no upregulation of thalamic β2*-nAChR availability during acute abstinence, which conflicts with postmortem2 and animal8, 79 studies.”
From β2-Nicotinic Acetylcholine Receptor Availability During Acute and Prolonged Abstinence From Tobacco Smoking (2009) · cites this paper as [2]
Postmortem studies of human brain have suggested that numbers of nAChRs are higher in smokers than in nonsmokers or former smokers.
“Postmortem studies of human brain have suggested that numbers of nAChRs are higher in smokers than in nonsmokers or former smokers (Benwell et al., 1988;Breese et al., 1997;Perry et al., 1999)”
From Human Tobacco Smokers in Early Abstinence Have Higher Levels of β<sub>2</sub>* Nicotinic Acetylcholine Receptors than Nonsmokers (2006) · cites this paper as Breese et al., 1997
A similar increase in nAChRs is found in autopsied brains from smokers.
“a similar increase is found in autopsied brains from smokers (Benwell et al., 1988;Breese et al., 1997;Perry et al., 1999)”
From Chronic Sazetidine-A at Behaviorally Active Doses Does Not Increase Nicotinic Cholinergic Receptors in Rodent Brain (2012) · cites this paper as Breese et al., 1997
Nicotine-induced up-regulation of nAChRs has been replicated in systems ranging from clonal cell lines to primary neurons in culture, mouse models, and smokers' brains.
“Nicotine-induced “up-regulation” has been replicated many times in systems ranging from clonal cell lines to primary neurons in culture, to mouse models, and to smokers’ brains (Breese et al., 1997; Court et al., 1998; Staley et al., 2006; Mukhin et al., 2008; Albuquerque et al., 2009; Lester et al., 2009).”
From Nicotine up-regulates α4β2 nicotinic receptors and ER exit sites via stoichiometry-dependent chaperoning (2011) · cites this paper as Breese et al., 1997
Human smokers show increased levels of nAChRs in functional magnetic resonance imaging and post mortem measurements.
“Human smokers also show increased levels of nAChRs in functional magnetic resonance imaging and post mortem measurements (6–9).”
From Nicotine is a selective pharmacological chaperone of acetylcholine receptor number and stoichiometry. Implications for drug discovery (2009) · cites this paper as [6]
The lack of thalamic increase in this study disagrees with a postmortem study that found Bmax in smokers almost twice that in nonsmokers.
“This lack of increase in the thalamus is not in agreement with the observations in a study of postmortem tissue showing values for the Bmax in smokers that were almost 2-fold those in nonsmokers (5).”
From Greater Nicotinic Acetylcholine Receptor Density in Smokers Than in Nonsmokers: A PET Study with 2-<sup>18</sup>F-FA-85380 (2008) · cites this paper as [5]
A possible explanation for the thalamic discrepancy is that this study's smokers smoked fewer cigarettes per day (15-30) than those in Breese et al. (10-60).
“A possible explanation is that the smokers in our study smoked fewer cigarettes/d (i.e., 15–30) than the smokers in the study by Breese et al. (10–60 cigarettes/d) (5).”
From Greater Nicotinic Acetylcholine Receptor Density in Smokers Than in Nonsmokers: A PET Study with 2-<sup>18</sup>F-FA-85380 (2008) · cites this paper as [5]
Postmortem tissue studies observed receptor densities in exsmokers similar to those in nonsmokers after more than 2 months of smoking cessation.
“Receptor densities in exsmokers that were similar to those in nonsmokers after more than 2 mo of smoking cessation were observed previously in postmortem tissue (5,6).”
From Greater Nicotinic Acetylcholine Receptor Density in Smokers Than in Nonsmokers: A PET Study with 2-<sup>18</sup>F-FA-85380 (2008) · cites this paper as [5]
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Czermak, C., Staley, J. K., Kasserman, S., Bois, F., Young, T., Henry, S., Tamagnan, G. D., Seibyl, J. P., Krystal, J. H., & Neumeister, A. (2008) · The International Journal of Neuropsychopharmacology · doi:10.1017/s1461145707008152 · Cited by 31 · see citing works
Yohn, N. L., Turner, J. R., & Blendy, J. A. (2014) · The Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.113.211706 · Cited by 28 · see citing works
Hoegberg, B. G., Lomazzo, E., Lee, N. H., & Perry, D. C. (2015) · Neuropharmacology · doi:10.1016/j.neuropharm.2015.08.015 · Cited by 17 · see citing works
- Authors
- Breese, C. R., Marks, M. J., Logel, J., Adams, C. E., Sullivan, B., Collins, A. C., & Leonard, S.
- Venue
- The Journal of Pharmacology and Experimental Therapeutics
- Publisher
- Elsevier BV
- Published
- 1997-07
- Volume
- 282
- Issue
- 1
- Pages
- 7-13
- ISSN
- 0022-3565 (ISSN-L)
- OpenAlex
- W1909773795
- Cited by
- 396
- References
- 40
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 5 · 2023: 6 · 2022: 6 · 2021: 3 · 2020: 29 · 2019: 8 · 2018: 7 · 2017: 4 · 2016: 18 · 2015: 20 · 2014: 14 · 2013: 19 · 2012: 17
- FWCI
- 4.74
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Pharmacology and Experimental Therapeutics (publishedVersion)
- PubMed (publishedVersion)
- PubMed
- Funders
- National Institutes of Health (5k05da000197-07)
- National Institute on Drug Abuse (DA 03194, DA00197, DA09457, R01DA003194, R01DA009457)
- 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
- nicotine, nicotinic acetylcholine receptors, smoking history, smoking cessation, receptor binding, hippocampus, thalamus, nicotine tolerance, nicotine dependence, postmortem brain
- MeSH terms
- Adult, Aged, Brain, Humans, Middle Aged, Nicotine, Receptors, Nicotinic, Smoking, Tritium
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.
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