Increased nicotinic receptors in brains from smokers: membrane binding and autoradiography studies
Abstract
Chronic administration of nicotine increases the density of neuronal cholinergic nicotinic receptors in cells and in rodent brain, and similar increases have been reported in brains from human smokers. To further examine this phenomenon, we measured nicotinic receptor binding sites in brain regions from matched populations of smokers and nonsmokers. We first measured binding of [3H](+/-)epibatidine ([3H]EB) and [3H]cytisine in homogenate preparations from samples of prefrontal and temporal cerebral cortex. Binding of each radioligand was significantly higher (250-300%) in both cortical regions from brains of smokers. Frozen sections from each of the cerebral cortical regions and the hippocampus were used for autoradiographic analysis of [3H]EB binding. In cerebral cortex, binding was most dense in layer VI in the prefrontal cortex and layers IV and VI in the temporal cortex. Densitometric analysis of [3H]EB binding sites revealed marked increases of 300 to 400% of control in all cortical regions examined from smokers' brains. Binding in the hippocampal formation was heterogeneously distributed, with dense areas of binding sites seen in the parasubiculum, subiculum, and molecular layer of the dentate gyrus, and the lacunosum-moleculare layer of the CA1/2. Binding of [3H]EB was significantly higher in all six regions of the hippocampus examined from brains of smokers compared with nonsmokers. These increases ranged from 160% of control in parasubiculum to 290% in the molecular layer of the dentate gyrus. The increase in nicotinic receptors in the cerebral cortex and hippocampus of smokers may modify the central nervous system effects of nicotine and contribute to an altered response of smokers to nicotine.
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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 Perry et al., 1999
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 Perry et al., 1999
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 [8]
During prolonged exposure to nicotine, there is decreased receptor degradation, presumably via endocytosis.
“During prolonged exposure to nicotine, there is deceased receptor degradation (presumably via endocytosis), and this mechanism for upregulation must be considered as an adjunct to SePhaChARNS (8,39,66,87).”
From Nicotine is a selective pharmacological chaperone of acetylcholine receptor number and stoichiometry. Implications for drug discovery (2009) · cites this paper as [8]
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“…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), and animals exposed to nicotine chronically exhibit increased levels of nAChRs in the brain (Marks et al., 1983, 1985, 1992;…”
BackgroundChronic Nicotine Exposure Upregulates Nicotinic Receptors by a Novel Mechanism
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Self-citationHussmann, G. P., Turner, J. R., Lomazzo, E., Venkatesh, R., Cousins, V., Xiao, Y., Yasuda, R. P., Wolfe, B. B., Perry, D. C., Rezvani, A. H., et al. (2012) · The Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.112.198085 · Cited by 34 · see citing works
Self-citationYohn, 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
Self-citationPentel, P. R., Keyler, D. E., Chen, Y., LeSage, M. G., Dufek, M. B., Le, C., & Leslie, F. M. (2006) · Neurotoxicology and Teratology · doi:10.1016/j.ntt.2006.08.001 · Cited by 14 · see citing works
- Authors
- Perry, D. C., Dávila-Garcı́a, M. I., Stockmeier, C. A., & Kellar, K. J.
- Affiliations
- Georgetown University (US)
- Corresponding author
- Kellar, Kenneth J.
- Venue
- The Journal of Pharmacology and Experimental Therapeutics
- Publisher
- Elsevier BV
- Published
- 1999-06
- Volume
- 289
- Issue
- 3
- Pages
- 1545-1552
- ISSN
- 0022-3565 (ISSN-L)
- OpenAlex
- W2139654665
- Cited by
- 362
- References
- 48
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 3 · 2023: 3 · 2022: 4 · 2021: 5 · 2020: 8 · 2019: 9 · 2018: 13 · 2017: 9 · 2016: 17 · 2015: 24 · 2014: 19 · 2013: 10 · 2012: 20
- FWCI
- 4.12
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Pharmacology and Experimental Therapeutics (publishedVersion)
- PubMed (publishedVersion)
- PubMed
- Funders
- National Institutes of Health (5r01ns034706-03, 5r01da006486-10)
- National Institute of Mental Health (MH-45488, R01MH045488)
- National Institute on Drug Abuse (DA-06486)
- National Institute of Neurological Disorders and Stroke (NS34706)
- 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, smoking, nicotine, receptor up-regulation, cerebral cortex, hippocampus, prefrontal cortex, temporal cortex, epibatidine binding, autoradiography
- MeSH terms
- Quinolizidine Alkaloids, Adult, Aged, Aging, Alkaloids, Autopsy, Autoradiography, Azocines, Brain, Cerebral Cortex, Female, Hippocampus, Humans, Male, Middle Aged, Neurons, Pyridines, Quinolizines, Radioligand Assay, Receptors, Nicotinic, Smoking, Temporal Lobe, Tritium, Prefrontal Cortex, Nicotinic Agonists, Bridged Bicyclo Compounds, Heterocyclic
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