Cotinine selectively activates a subpopulation of α3/α6β2* nicotinic receptors in monkey striatum
Open accessAbstract
The nicotine metabolite cotinine is an abundant long-lived bio-active compound that may contribute to the overall physiological effects of tobacco use. Although its mechanism of action in the central nervous system has not been extensively investigated, cotinine is known to evoke dopamine release in the nigrostriatal pathway through an interaction at nicotinic receptors (nAChRs). Because considerable evidence now demonstrates the presence of multiple nAChRs in the striatum, the present experiments were done to determine the subtypes through which cotinine exerts its effects in monkeys, a species that expresses similar densities of striatal alpha4beta2* (nAChR containing the alpha4 and beta2 subunits, but not alpha3 or alpha6) and alpha3/alpha6beta2* (nAChR composed of the alpha3 or alpha6 subunits and beta2) nAChRs. Competition binding studies showed that cotinine interacts with both alpha4beta2* and alpha3/alpha6beta2* nAChR subtypes in the caudate, with cotinine IC(50) values for inhibition of 5-[(125) I]iodo-3-[2(S)-azetinylmethoxy]pyridine-2HCl ([(125)I]A-85380) and (125)I-alpha-conotoxinMII binding in the micromolar range. This interaction at the receptor level is of functional significance because cotinine stimulated both alpha4beta2* and alpha3/alpha6beta2* nAChR [(3)H]dopamine release from caudate synaptosomes. Our results unexpectedly showed that nicotine evokes [(3)H]dopamine release from two alpha3/alpha6beta2* nAChR populations, one of which was sensitive to cotinine and the other was not. This cotinine-insensitive subtype was only present in the medial caudate and was preferentially lost with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced nigrostriatal damage. In contrast, cotinine and nicotine elicited equivalent levels of alpha4beta2* nAChR-mediated dopamine release. These data demonstrate that cotinine functionally discriminates between two alpha3/alpha6beta2* nAChRs in monkey striatum, with the cotinine-insensitive alpha3/alpha6beta2* nAChR preferentially vulnerable to nigrostriatal damage.
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Cotinine stimulates nAChRs and may have biological effects.
“The rather high circulating plasma cotinine levels after nicotine ingestion, coupled with findings that cotinine stimulates nAChRs, has prompted the suggestion that cotinine per se may have biological effects (Dwoskin et al., 1999;O'Leary et al., 2008).”
From Nicotinic receptor-mediated reduction in l-DOPA-induced dyskinesias may occur via desensitization (2010) · cites this paper as O'Leary et al., 2008
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- Authors
- O’Leary, K., Parameswaran, N., McIntosh, J. M., & Quik, M.
- Affiliations
- Parkinson's Institute and Clinical Center (US)
- ORCID
- McIntosh, J. Michael
- Venue
- The Journal of Pharmacology and Experimental Therapeutics
- Publisher
- Elsevier BV
- Published
- 2008-05
- Volume
- 325
- Issue
- 2
- Pages
- 646-654
- ISSN
- 0022-3565 (ISSN-L)
- PMC
- PMC3134143
- OpenAlex
- W2103153047
- Cited by
- 45
- References
- 49
- Citations by year
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- FWCI
- 1.51
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Pharmacology and Experimental Therapeutics (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Johns Hopkins University
- National Institute of Mental Health (MH53631, R01MH053631, R29MH053631)
- National Institute on Drug Abuse (R01DA012242, DA12242)
- National Institute of General Medical Sciences (P01GM048677)
- National Institute of Neurological Disorders and Stroke (R01NS047162, NS42091, NS47162, 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
- cotinine, nicotinic acetylcholine receptors, alpha4beta2 nAChR, striatum, caudate nucleus, dopamine release, nigrostriatal pathway, MPTP, receptor subtypes
- MeSH terms
- Animals, Azetidines, Brain, Cocaine, Cotinine, Dopamine, Female, Nicotine, Receptors, Nicotinic, Saimiri, Dopamine Agents, 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Nicotinic Agonists, Nicotinic Antagonists, Conotoxins
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.
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