The subtypes of nicotinic acetylcholine receptors on dopaminergic terminals of mouse striatum
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This review summarizes studies that attempted to determine the subtypes of nicotinic acetylcholine receptors (nAChR) expressed in the dopaminergic nerve terminals in the mouse. A variety of experimental approaches has been necessary to reach current knowledge of these subtypes, including in situ hybridization, agonist and antagonist binding, function measured by neurotransmitter release from synaptosomal preparations, and immunoprecipitation by selective antibodies. Early developments that facilitated this effort include the radioactive labeling of selective binding agents, such as [(125)I]-alpha-bungarotoxin and [(3)H]-nicotine, advances in cloning the subunits, and expression and evaluation of function of combinations of subunits in Xenopus oocytes. The discovery of epibatidine and alpha-conotoxin MII (alpha-CtxMII), and the development of nAChR subunit null mutant mice have been invaluable in determining which nAChR subunits are important for expression and function in mice, as well as allowing validation of the specificity of subunit specific antibodies. These approaches have identified five nAChR subtypes of nAChR that are expressed on dopaminergic nerve terminals. Three of these contain the alpha6 subunit (alpha4alpha6beta2beta3, alpha6beta2beta3, alpha6beta2) and bind alpha-CtxMII with high affinity. One of these three subtypes (alpha4alpha6beta2beta3) also has the highest sensitivity to nicotine of any native nAChR that has been studied, to date. The two subtypes that do not have high affinity for alpha-CtxMII (alpha4beta2, alpha4alpha5beta2) are somewhat more numerous than the alpha6* subtypes, but do bind nicotine with high affinity. Given that our first studies detected readily measured differences in sensitivity to agonists and antagonists among these five nAChR subtypes, it seems likely that subtype selective compounds could be developed that would allow therapeutic manipulation of diverse nAChRs that have been implicated in a number of human conditions.
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The α4β2*, α6β2*, and α7 nAChR subtypes have been implicated in striatal function and influence striatal dopamine release.
“All three nAChR subtypes (␣42*, ␣62*, and ␣7) have been implicated in striatal function and shown to influence striatal dopamine release (Grady et al., 2007).”
From Nicotinic receptor-mediated reduction in l-DOPA-induced dyskinesias may occur via desensitization (2010) · cites this paper as Grady et al., 2007
α4β2* nAChRs in the striatum are 80% localized postsynaptically on GABAergic neurons where they modulate GABA release and 20% presynaptically on dopaminergic terminals involved in regulating dopamine release.
“In addition, they are present in the striatum, with 80% localized postsynaptically on GABAergic neurons where they modulate GABA release and 20% presynaptically on dopaminergic terminals that are involved in regulating dopamine release (Grady et al., 2007;Quik et al., 2008).”
From Nicotinic receptor-mediated reduction in l-DOPA-induced dyskinesias may occur via desensitization (2010) · cites this paper as Grady et al., 2007
α6β2* nAChRs localized to catecholaminergic neurons may also be relevant for the observed effects of nicotine on L-DOPA-induced AIMs.
“The ␣62* nAChRs localized to catecholaminergic neurons may also be of relevance for the observed effects of nicotine on L-DOPA-induced AIMs (Grady et al., 2007;Quik et al., 2008).”
From Nicotinic receptor-mediated reduction in l-DOPA-induced dyskinesias may occur via desensitization (2010) · cites this paper as Grady et al., 2007
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- Authors
- Grady, S. R., Salminen, O., Laverty, D. C., Whiteaker, P., McIntosh, J. M., Collins, A. C., & Marks, M. J.
- Affiliations
- University of Colorado Boulder (US)
- University of Helsinki (FI)
- University of Utah (US)
- Corresponding author
- Grady, Sharon R.
- Venue
- Biochemical Pharmacology
- Publisher
- Elsevier BV
- Published
- 2007-10
- Volume
- 74
- Issue
- 8
- Pages
- 1235-1246
- ISSN
- 0006-2952 (ISSN-L)
- PMC
- PMC2735219
- OpenAlex
- W1970133822
- Cited by
- 252
- References
- 131
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 6 · 2023: 10 · 2022: 9 · 2021: 7 · 2020: 13 · 2019: 13 · 2018: 8 · 2017: 13 · 2016: 12 · 2015: 10 · 2014: 19 · 2013: 12 · 2012: 19
- FWCI
- 1.88
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Biochemical Pharmacology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Drug Abuse (U19DA019375, DA 015663, DA 03194, DA 019375, R01DA017279, P30DA015663, R01DA003194, R01DA012242, DA12242)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
- Keywords
- nicotinic acetylcholine receptors, dopaminergic terminals, striatum, receptor subtypes, alpha6 subunit, alpha-conotoxin MII, epibatidine, nicotine sensitivity, receptor subunit composition
- MeSH terms
- Animals, Bungarotoxins, Corpus Striatum, Dopamine, Pyridines, Receptors, Nicotinic, Bridged Bicyclo Compounds, Heterocyclic, Conotoxins, Mice
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