Striatal cholinergic interneurons drive GABA release from dopamine terminals
Open accessAbstract
Striatal cholinergic interneurons are implicated in motor control, associative plasticity, and reward-dependent learning. Synchronous activation of cholinergic interneurons triggers large inhibitory synaptic currents in dorsal striatal projection neurons, providing one potential substrate for control of striatal output, but the mechanism for these GABAergic currents is not fully understood. Using optogenetics and whole-cell recordings in brain slices, we find that a large component of these inhibitory responses derive from action-potential-independent disynaptic neurotransmission mediated by nicotinic receptors. Cholinergically driven IPSCs were not affected by ablation of striatal fast-spiking interneurons but were greatly reduced after acute treatment with vesicular monoamine transport inhibitors or selective destruction of dopamine terminals with 6-hydroxydopamine, indicating that GABA release originated from dopamine terminals. These results delineate a mechanism in which striatal cholinergic interneurons can co-opt dopamine terminals to drive GABA release and rapidly inhibit striatal output neurons.
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Several groups found that vGluT and VAChT function synergistically, and depletion of one transporter or neurotransmitter also depletes loading and release of the other.
“Interestingly, several groups have found that vGluT and VAChT function synergistically and that depletion of one transporter or neurotransmitter also depletes loading and release of the other.21,22,63,69”
From Synaptic and circuit functions of multitransmitter neurons in the mammalian brain (2023) · cites this paper as [63]
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References 33 · Cited by 169
- Authors
- Nelson, A. B., Hammack, N., Yang, C. F., Shah, N. M., Seal, R. P., & Kreitzer, A. C.
- Affiliations
- Gladstone Institutes (US)
- University of California, San Francisco (US)
- University of Pittsburgh (US)
- Corresponding author
- Kreitzer, Anatol C.
- ORCID
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2014-04
- Volume
- 82
- Issue
- 1
- Pages
- 63-70
- ISSN
- 0896-6273 (ISSN-L)
- PMC
- PMC3976769
- OpenAlex
- W2118021908
- Cited by
- 169
- References
- 33
- Citations by year
- 2026: 5 · 2025: 9 · 2024: 10 · 2023: 5 · 2022: 11 · 2021: 10 · 2020: 13 · 2019: 16 · 2018: 12 · 2017: 15 · 2016: 31 · 2015: 17 · 2014: 15
- FWCI
- 11.88
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (R01NS078435, R01NS083872, K08NS081001, R01NS064984, R01NS082650, R01NS049488)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Keywords
- striatal cholinergic interneurons, GABA release, dopaminergic terminals, nicotinic acetylcholine receptors, inhibitory postsynaptic currents, striatal projection neurons, fast-spiking interneurons, 6-hydroxydopamine, optogenetics
- MeSH terms
- Channelrhodopsins, Action Potentials, Animals, Choline O-Acetyltransferase, Corpus Striatum, Dopamine, gamma-Aminobutyric Acid, Interneurons, Mice, Inbred C57BL, Mice, Transgenic, Parvalbumins, Receptors, Dopamine D1, Neurotransmitter Agents, Patch-Clamp Techniques, Potassium Channel Blockers, Sodium Channel Blockers, Mice, Inhibitory Postsynaptic Potentials, In Vitro Techniques
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