The DOI matches its Crossref record; 47 of the 48 references it cites were found in a registry or an index.
Nicotinic agonists stimulate acetylcholine release from mouse interpeduncular nucleus: a function mediated by a different nAChR than dopamine release from striatum
Abstract
Acetylcholine release stimulated by nicotinic agonists was measured as radioactivity released from perfused synaptosomes prepared from mouse interpeduncular nucleus (IPN) that had been loaded with [(3)H]choline. Agonist-stimulated release was dependent upon external calcium and over 90% of released radioactivity was acetylcholine. The release process was characterized by dose response curves for 13 agonists and inhibition curves for six antagonists. alpha-Conotoxin MII did not inhibit this release, while alpha-conotoxin AuIB inhibited 50% of agonist-stimulated release. Comparison of this process with [(3)H]dopamine release from mouse striatal synaptosomes indicated that different forms of nicotinic acetylcholine receptors (nAChRs) may mediate these processes. This was confirmed by assays using mice homozygous for the beta 2 subunit null mutation. The deletion of the beta 2 subunit had no effect on agonist-stimulated acetylcholine release, but abolished agonist-stimulated release of dopamine from striatal synaptosomes. Mice heterozygous for the beta 2 subunit null mutation showed decreased dopamine release evoked by L-nicotine with no apparent change in EC(50) value, as well as similar decreases in both transient and persistent phases of release with no changes in desensitization rates.
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In the citing paper
“Knockout of the β2 subunit abolishes nicotine-mediated DA release (Picciotto et al. 1998;Grady et al. 2001), nicotine-induced locomotor activation (King et al. 2004), nicotine selfadministration (Picciotto et al. 1998;Maskos et al. 2005), and nicotine place preference (Walters et al. 2006;Brunzell et al. 2009;Mineur et al. 2009a).”
From Mechanisms of Nicotine Addiction (2021) · cites this paper as Grady et al. 2001
In the citing paper
“Nicotinic modulation of neurotransmitter release is often subtype-specific and this specificity can vary across brain areas, with distinct nAChRs coupling to release of glutamate (α7) vs. GABA (α4β2*) (Mansvelder et al., 2002) or DA (α4/α6β2*) vs. ACh (α3β4*) (Grady et al., 2001) in the VTA, while β2* nAChRs can modulate the release of glutamate from thalamo-cortical projections (Parikh et al., 20”
From Acetylcholine as a Neuromodulator: Cholinergic Signaling Shapes Nervous System Function and Behavior (2012) · cites this paper as Grady et al., 2001
Citations
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Acetylcholine as a Neuromodulator: Cholinergic Signaling Shapes Nervous System Function and Behavior
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Metadata
- Authors
- Grady, S. R., Meinerz, N. M., Cao, J., Reynolds, A. M., Picciotto, M. R., Changeux, J., McIntosh, J. M., Marks, M. J., & Collins, A. C.
- Affiliations
- University of Colorado Boulder (US)
- Yale University (US)
- Centre National de la Recherche Scientifique (FR)
- University of Utah (US)
- Corresponding author
- Collins, Allan C.
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2001-01
- Volume
- 76
- Issue
- 1
- Pages
- 258-268
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W1515685619
- Cited by
- 156
- References
- 48
- Citations by year
- 2025: 2 · 2024: 2 · 2023: 1 · 2022: 1 · 2021: 2 · 2020: 2 · 2019: 4 · 2018: 3 · 2017: 5 · 2016: 4 · 2015: 2 · 2014: 11 · 2013: 3 · 2012: 7
- FWCI
- 4.54
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Mental Health (MH53631)
- National Institute on Drug Abuse (DA 03194, 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 › Public Health, Environmental and Occupational Health › Smoking Behavior and Cessation
- Keywords
- nicotinic acetylcholine receptors, acetylcholine release, interpeduncular nucleus, dopamine release, striatum, alpha-conotoxin MII, nicotinic agonists, calcium-dependent release, receptor desensitization, synaptosomes
- MeSH terms
- Quinolizidine Alkaloids, Acetylcholine, Alkaloids, Animals, Azocines, Calcium, Choline, Corpus Striatum, Dopamine, Dose-Response Relationship, Drug, Female, Heterozygote, Homozygote, Male, Mesencephalon, Mice, Inbred C57BL, Mice, Mutant Strains, Quinolizines, Receptors, Nicotinic, Synaptosomes, Presynaptic Terminals, Nicotinic Agonists, Nicotinic Antagonists, Conotoxins, Protein Subunits, Mice
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