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Chronic nicotine and mecamylamine treatment increase brain nicotinic receptor binding without changing alpha 4 or beta 2 mRNA levels
Abstract
It has recently been shown using regionally dissected tissue that both chronic mecamylamine treatment and chronic nicotine treatment increase the number of [3H]-nicotine binding sites in mouse brain, and that additive increases in the number of binding sites is observed after cotreatment with the two drugs. The studies reported here extend these findings by using quantitative autoradiographic methods to analyze the brains of chronically treated mice at a finer anatomical level of resolution. DBA/2 mice were chronically infused (i.v.) with saline, 4.0 mg/ kg/hr nicotine, 4.0 mg/kg/hr mecamylamine or both drugs for 7 days. The brains of these mice were subsequently analyzed to determine the effects of chronic drug treatment on [3H]-nicotine binding and on the levels of mRNA encoding the nicotinic receptor subunits, alpha 4 and beta 2. [3H]-Nicotine binding was increased in 37 of 46 brain regions after chronic nicotine treatment (average increase = 66.5%), in 41 of 46 regions after chronic mecamylamine treatment (average increase = 56.5%), and in 45 of 46 brain regions after chronic treatment with both drugs (average increase = 107.1%). The changes in [3H]-nicotine binding produced by the two drugs across brain regions were highly (r = 0.98) and significantly correlated. These results are consistent with the proposal that the same receptors are affected by agonist or antagonist treatment. Chronic treatment had no significant effect on the levels of alpha 4 or beta 2 mRNA as measured by in situ hybridization. Therefore, the increases in [3H]-nicotine binding do not arise from changes in the steady-state levels of either alpha 4 or beta 2 mRNA which are believed to encode the subunits of this nicotinic receptor subtype.
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In the citing paper
“Our finding replicates prior in situ hybridization work that found no chronic nicotine-associated change in hippocampal (and other areas) α4 or β2 mRNA levels (Marks et al., 1992; Pauly et al., 1996)”
From The duration of nicotine withdrawal-associated deficits in contextual fear conditioning parallels changes in hippocampal high affinity nicotinic acetylcholine receptor upregulation (2012) · cites this paper as Pauly et al., 1996
In the citing paper
“Upregulation induced in animal models and transfected cells by chronic nicotine is certainly not transcriptional and is probably post-translational (47).”
From Nicotine is a selective pharmacological chaperone of acetylcholine receptor number and stoichiometry. Implications for drug discovery (2009) · cites this paper as [47]
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Metadata
- Authors
- Pauly, J. R., Marks, M. J., Robinson, S. F., van de Kamp, J. L., & Collins, A. C.
- Affiliations
- Augusta University (US)
- Venue
- The Journal of Pharmacology and Experimental Therapeutics
- Publisher
- Elsevier BV
- Published
- 1996-07
- Volume
- 278
- Issue
- 1
- Pages
- 361-369
- ISSN
- 0022-3565 (ISSN-L)
- OpenAlex
- W1820461132
- Cited by
- 126
- References
- 0
- Citations by year
- 2022: 2 · 2021: 1 · 2020: 1 · 2019: 3 · 2018: 1 · 2017: 2 · 2016: 5 · 2015: 9 · 2014: 3 · 2013: 8 · 2012: 7
- FWCI
- 1.77
- 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, R01DA003194)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Smoking Behavior and Cessation
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- nicotinic acetylcholine receptors, chronic nicotine treatment, mecamylamine, receptor mRNA expression, receptor up-regulation, DBA/2 mice
- MeSH terms
- Animals, Autoradiography, Binding, Competitive, Brain, Female, Mecamylamine, Mice, Inbred DBA, Nicotine, RNA, Messenger, Up-Regulation, Mice
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