Increases in α4* but not α3*/α6* nicotinic receptor sites and function in the primate striatum following chronic oral nicotine treatment
Abstract
Knowledge of the effects of chronic nicotine is critical considering its widespread use in tobacco products and smoking cessation therapies. Although nicotine is well known to up-regulate alpha4* nAChR sites and function in the cortex, its actions in the striatum are uncertain because of the presence of multiple subtypes with potentially opposing effects. We therefore investigated the effect of long-term nicotine treatment on nAChR sites and function in the primate striatum, which offers the advantage of similar proportions of alpha3*/alpha6* and alpha4* nAChRs. Nicotine was given in drinking water, which resembles smoking in its intermittent but chronic delivery. Plasma nicotine and cotinine levels were similar to smokers. Chronic nicotine treatment (> 6 months) enhanced alpha4* nAChR-evoked [(3)H]dopamine release in striatal subregions, with an overall pattern of increase throughout the striatum when normalized to uptake. This increase correlated with elevated striatal alpha4* nAChRs. Under the same conditions, striatal alpha3*/alpha6* nAChR sites and function were decreased or unchanged. These divergent actions of chronic nicotine treatment on alpha4* versus alpha6* nAChRs, as well as effects on dopamine uptake, allow for a complex control of striatal activity to maintain dopaminergic function. Such knowledge is important for understanding nicotine dependence and the consequences of nicotine administration for the treatment of neurological disorders.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
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?
Different β2*-subunit combinations appear to be differentially regulated by nicotine, with α3/α6 and α6α4β2* and α5α4β2* not upregulating or decreasing in response to nicotine while α6β2 (nonα4) nAChR increase in response to nicotine.
“Importantly, different β2*-subunit combinations appear to be differentially regulated by nicotine, with α3/α6 and α6α4β2* and α5α4β2* not upregulating or decreasing in response to nicotine38, 85-88 while α6β2 (nonα4) nAChR increase in response to nicotine88.”
From β2-Nicotinic Acetylcholine Receptor Availability During Acute and Prolonged Abstinence From Tobacco Smoking (2009) · cites this paper as [87]
Cites
Flores, C. M., Rogers, S. W., Pabreza, L. A., Wolfe, B. B., & Kellar, K. J. (1992) · Molecular Pharmacology · doi:10.1016/s0026-895x(25)08832-7 · Cited by 880 · see citing works
Nicotinic Cholinergic Receptor Binding Sites in the Brain: Regulation in Vivo
Schwartz, R. D., & Kellar, K. J. (1983) · Science · doi:10.1126/science.6828889 · Cited by 479 · see citing works
Desensitization of nicotinic ACh receptors: shaping cholinergic signaling
GINIATULLIN, R., NISTRI, A., & YAKEL, J. (2005) · Trends in Neurosciences · doi:10.1016/j.tins.2005.04.009 · Cited by 357 · see citing works
Whiteaker, P., Sharples, C. G. V., & Wonnacott, S. (1998) · Molecular Pharmacology · doi:10.1016/s0026-895x(24)13263-4 · Cited by 152 · see citing works
Nguyen, H. N., Rasmussen, B. A., & Perry, D. C. (2003) · The Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.103.056408 · Cited by 148 · see citing works
Grady, S. R., Murphy, K. L., Cao, J., Marks, M. J., McIntosh, J. M., & Collins, A. C. (2002) · The Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.301.2.651 · Cited by 110 · see citing works
Self-citationPietilä, K., Lähde, T., Attila, M., Ahtee, L., & Nordberg, A. (1998) · Naunyn-Schmiedeberg's Archives of Pharmacology · doi:10.1007/pl00005152 · Cited by 67 · see citing works
Schoedel, K. A., Sellers, E. M., Palmour, R., & Tyndale, R. F. (2003) · Molecular Pharmacology · doi:10.1124/mol.63.1.96 · Cited by 64 · see citing works
Self-citationVisanji, N. P., Mitchell, S. N., O'Neill, M. J., & Duty, S. (2006) · Neuropharmacology · doi:10.1016/j.neuropharm.2005.07.013 · Cited by 25 · see citing works
Flagged first, then by citations
Cited by
Sorted by citations
Cosgrove, K. P., Batis, J., Bois, F., Maciejewski, P. K., Esterlis, I., Kloczynski, T., Stiklus, S., Krishnan-Sarin, S., O’Malley, S., Perry, E., et al. (2009) · Archives of General Psychiatry · doi:10.1001/archgenpsychiatry.2009.41 · Cited by 159 · see citing works
Up-regulation of Nicotinic Receptors by Nicotine Varies with Receptor Subtype
Walsh, H., Govind, A. P., Mastro, R., Hoda, J. C., Bertrand, D., Vallejo, Y., & Green, W. N. (2008) · Journal of Biological Chemistry · doi:10.1074/jbc.m703432200 · Cited by 87 · see citing works
Perez, X. A., Bordia, T., McIntosh, J. M., Grady, S. R., & Quik, M. (2008) · Molecular Pharmacology · doi:10.1124/mol.108.048843 · Cited by 77 · see citing works
Self-citationTumkosit, P., Kuryatov, A., Luo, J., & Lindstrom, J. (2006) · Molecular Pharmacology · doi:10.1124/mol.106.027326 · Cited by 73 · see citing works
Perez, X. A., O’Leary, K. T., Parameswaran, N., McIntosh, J. M., & Quik, M. (2009) · Molecular Pharmacology · doi:10.1124/mol.108.053801 · Cited by 38 · see citing works
Self-citation
- Authors
- McCallum, S. E., Parameswaran, N., Bordia, T., Fan, H., Tyndale, R. F., Langston, J. W., McIntosh, J. M., & Quik, M.
- Affiliations
- Parkinson's Institute and Clinical Center (US)
- Johns Hopkins University (US)
- Centre for Addiction and Mental Health (CA)
- University of Utah (US)
- Corresponding author
- Quik, Maryka
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2006-01-26
- Volume
- 96
- Issue
- 4
- Pages
- 1028-1041
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W1579854617
- Cited by
- 44
- References
- 9
- Citations by year
- 2020: 2 · 2019: 2 · 2018: 1 · 2015: 6 · 2014: 5 · 2013: 2 · 2012: 1
- FWCI
- 2.44
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute of Mental Health (MH53631, R01MH053631)
- National Institute on Drug Abuse (R01DA012242, DA12242)
- National Institute of Neurological Disorders and Stroke (R01NS047162, NS42091, NS47162, R01NS042091)
- National Institute of Environmental Health Sciences (U54ES012077, ES12077)
- 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
- chronic nicotine, nicotinic acetylcholine receptors, alpha4 nAChR, striatum, dopamine release, dopamine uptake, receptor up-regulation, primate brain, nicotine dependence, smoking
- MeSH terms
- Administration, Oral, Animals, Biological Transport, Corpus Striatum, Cotinine, Dopamine, Nicotine, Putamen, Receptors, Nicotinic, Saimiri, Synaptosomes
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
