The neuronal nicotinic acetylcholine receptors α4* and α6* differentially modulate dopamine release in mouse striatal slices
Open accessAbstract
Striatal dopamine (DA) plays a major role in the regulation of motor coordination and in the processing of salient information. We used voltammetry to monitor DA-release evoked by electrical stimulation in striatal slices, where interneurons continuously release acetylcholine. Use of the alpha6-selective antagonist alpha-conotoxin MII[E11A] and alpha4 knockout mice enabled identification of two populations of DA-ergic fibers. The first population had a low action potential threshold, and action potential-evoked DA-release from these fibers was modulated by alpha6. The second population had a higher action potential threshold, and only alpha4(non-alpha6) modulated action potential-evoked DA-release. Striatal DA-ergic neurons fire in both tonic and phasic patterns. When stimuli were applied in a train to mimic phasic firing, more DA-release was observed in alpha4 knockout versus wild-type mice. Furthermore, block of alpha4(non-alpha6), but not of alpha6, increased DA release evoked by a train. These results indicate that there are different classes of striatal DA-ergic fibers that express different subtypes of nicotinic receptors.
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Nicotinic regulation of dopamine release likely involves an interplay between receptor activation and desensitization, and desensitization produces an effective channel block similar to that seen with nAChR antagonists.
“In addition, studies using cyclic voltametry indicate that this regulation of dopamine release most likely represents a complex interplay between nicotinic receptor activation and desensitization (Exley et al., 2008;Meyer et al., 2008;Perez et al., 2008)”
From Nicotinic receptor-mediated reduction in l-DOPA-induced dyskinesias may occur via desensitization (2010) · cites this paper as Meyer et al., 2008
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References 61 · Cited by 58
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- Bordia T, Grady SR, McIntosh JM, Quik M. Nigrostriatal damage preferentially decreases a subpopulation of {alpha}6{beta}2* nAChRs in mouse, monkey and Parkinson's disease striatum. Mol Pharmacol. 2007b doi: 10.1124/mol.107.035998. [DOI] [PubMed] [Google Scholar] · DOI
- Authors
- Meyer, E. L., Yoshikami, D., & McIntosh, J. M.
- Affiliations
- University of Utah (US)
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2008-02
- Volume
- 105
- Issue
- 5
- Pages
- 1761-1769
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- PMC
- PMC2527994
- OpenAlex
- W2016683069
- Cited by
- 58
- References
- 61
- Citations by year
- 2024: 3 · 2021: 2 · 2019: 2 · 2018: 1 · 2017: 2 · 2016: 5 · 2015: 3 · 2014: 3 · 2013: 4 · 2012: 8
- FWCI
- 3.40
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of Mental Health (MH53631, R01MH053631, R29MH053631)
- National Institute on Drug Abuse (DA 015663, P30DA015663)
- National Institute of General Medical Sciences (P01GM048677, GM48677)
- 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
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- nicotinic acetylcholine receptors, alpha4 subunit, alpha6 subunit, striatal dopamine release, striatal interneurons, alpha-conotoxin MII, action potential threshold, phasic firing, tonic firing, striatal slices
- MeSH terms
- Animals, Corpus Striatum, Dopamine, Electric Stimulation, Evoked Potentials, Mice, Inbred C57BL, Receptors, Nicotinic, Mice, Knockout, Mice
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