In vivo activation of midbrain dopamine neurons via sensitized, high-affinity α6 nicotinic acetylcholine receptors
Open accessAbstract
Alpha6-containing (alpha6*) nicotinic ACh receptors (nAChRs) are selectively expressed in dopamine (DA) neurons and participate in cholinergic transmission. We generated and studied mice with gain-of-function alpha6* nAChRs, which isolate and amplify cholinergic control of DA transmission. In contrast to gene knockouts or pharmacological blockers, which show necessity, we show that activating alpha6* nAChRs and DA neurons is sufficient to cause locomotor hyperactivity. alpha6(L9'S) mice are hyperactive in their home cage and fail to habituate to a novel environment. Selective activation of alpha6* nAChRs with low doses of nicotine, by stimulating DA but not GABA neurons, exaggerates these phenotypes and produces a hyperdopaminergic state in vivo. Experiments with additional nicotinic drugs show that altering agonist efficacy at alpha6* provides fine tuning of DA release and locomotor responses. alpha6*-specific agonists or antagonists may, by targeting endogenous cholinergic mechanisms in midbrain or striatum, provide a method for manipulating DA transmission in neural disorders.
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A smaller population of α6β2* nAChRs is restricted to CNS catecholaminergic neurons, including nigrostriatal neurons, and may be involved in reward, addiction, and motor activity.
“There is also a smaller population of ␣62* nAChRs, which is restricted in localization to CNS catecholaminergic neurons, including those in the nigrostriatal pathway, which may be involved in reward, addiction, and motor activity (Drenan et al., 2008;Pons et al., 2008).”
From Nicotinic receptor-mediated reduction in l-DOPA-induced dyskinesias may occur via desensitization (2010) · cites this paper as Drenan et al., 2008
The addictive effects of nicotine are mediated primarily through stimulation of nicotinic acetylcholine receptors in the VTA.
“particularly because the addictive effects of nicotine are mediated primarily through stimulation of nAChRs in the VTA (Drenan et al., 2008; Maskos et al., 2005; McGranahan et al., 2011; Picciotto et al., 1998).”
From Acetylcholine as a Neuromodulator: Cholinergic Signaling Shapes Nervous System Function and Behavior (2012) · cites this paper as Drenan et al., 2008
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- Authors
- Drenan, R. M., Grady, S. R., Whiteaker, P., McClure-Begley, T., McKinney, S., Miwa, J. M., Bupp, S., Heintz, N., McIntosh, J. M., Bencherif, M., Marks, M. J., & Lester, H. A.
- Affiliations
- California Institute of Technology (US)
- University of Colorado Boulder (US)
- Howard Hughes Medical Institute (US)
- University of Utah (US)
- Corresponding author
- Lester, Henry A.
- ORCID
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2008-10
- Volume
- 60
- Issue
- 1
- Pages
- 123-136
- ISSN
- 0896-6273 (ISSN-L)
- PMC
- PMC2632732
- OpenAlex
- W1968189433
- Cited by
- 197
- References
- 60
- Citations by year
- 2026: 5 · 2025: 7 · 2024: 6 · 2023: 3 · 2022: 3 · 2021: 3 · 2020: 6 · 2019: 8 · 2018: 9 · 2017: 12 · 2016: 12 · 2015: 9 · 2014: 26 · 2013: 13 · 2012: 16
- FWCI
- 8.08
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- CaltechAUTHORS (California Institute of Technology) (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- National Institutes of Health (5t32ns007251-22)
- National Institute of Mental Health (MH53631, R01MH053631, R29MH053631)
- National Institute on Drug Abuse (DA-19375, U19DA019375, DA 03194, DA17279, R01DA017279, F32DA021492, R01DA003194, DA09121, R01DA012242, R01DA009121, DA12242, DA021492)
- National Institute of General Medical Sciences (P01GM048677, GM48677)
- National Institute of Neurological Disorders and Stroke (T32 NS-007251, NS 11756, NS007251, R01NS011756)
- 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
- dopaminergic neurons, midbrain, locomotor hyperactivity, nicotine, hyperdopaminergic state, striatum, neuropsychiatric disorders
- MeSH terms
- Animals, Dopamine, Mesencephalon, Mice, Transgenic, Synaptic Transmission, Neurons, Receptors, Nicotinic, Recombination, Genetic, Chromosomes, Artificial, Bacterial, Mice
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 ›
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