Nicotinic agonists stimulate acetylcholine release from mouse interpeduncular nucleus: a function mediated by a different nAChR than dopamine release from striatum

Grady, Sharon R.; Meinerz, Natalie M.; Cao, Jian; Reynolds, Andrew M.; Picciotto, Marina R.; Changeux, Jean‐Pierre; McIntosh, J. Michael; Marks, Michael J.; Collins, Allan C.

doi:10.1046/j.1471-4159.2001.00019.x

Cited by 158Nicotinic Acetylcholine Receptors StudyNeuroscience and Neuropharmacology ResearchSmoking Behavior and Cessation

Nicotinic agonists stimulate acetylcholine release from mouse interpeduncular nucleus: a function mediated by a different nAChR than dopamine release from striatum

Grady, Sharon R., Meinerz, Natalie M., Cao, Jian, Reynolds, Andrew M., Picciotto, Marina R., Changeux, Jean‐Pierre, McIntosh, J. Michael, Marks, Michael J. +1 more·2001·Journal of Neurochemistry

DOI 10.1046/j.1471-4159.2001.00019.x

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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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Knockout of the β2 subunit abolishes nicotine-mediated DA release, nicotine-induced locomotor activation, nicotine self-administration, and nicotine place preference.
“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
Nicotinic modulation of neurotransmitter release is often subtype-specific and this specificity can vary across brain areas.
“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

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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.
ORCID: Cao, Jian
Picciotto, Marina R.
Changeux, Jean‐Pierre
McIntosh, J. Michael
Marks, Michael J.
Venue: Journal of Neurochemistry
Publisher: Wiley
Published: 2001-01
Volume: 76
Issue: 1
Pages: 258-268
ISSN: 0022-3042 (ISSN-L)
1471-4159
DOI: 10.1046/j.1471-4159.2001.00019.x
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
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor, 2839 d)
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 › Physiology › 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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Nicotinic agonists stimulate acetylcholine release from mouse interpeduncular nucleus: a function mediated by a different nAChR than dopamine release from striatum

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