The DOI matches its Crossref record; 37 of the 37 references it cites were found in a registry or an index.
Cholinergic interneurons in the nucleus accumbens regulate depression-like behavior
Open accessAbstract
A large number of studies have demonstrated that the nucleus accumbens (NAC) is a critical site in the neuronal circuits controlling reward responses, motivation, and mood, but the neuronal cell type(s) underlying these processes are not yet known. Identification of the neuronal cell types that regulate depression-like states will guide us in understanding the biological basis of mood and its regulation by diseases like major depressive disorder. Taking advantage of recent findings demonstrating that the serotonin receptor chaperone, p11, is an important molecular regulator of depression-like states, here we identify cholinergic interneurons (CINs) as a primary site of action for p11 in the NAC. Depression-like behavior is observed in mice after decrease of p11 levels in NAC CINs. This phenotype is recapitulated by silencing neuronal transmission in these cells, demonstrating that accumbal cholinergic neuronal activity regulates depression-like behaviors and suggesting that accumbal CIN activity is crucial for the regulation of mood and motivation.
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In the citing paper
“Mice lacking p11 [162], p11 reductions in NAc [163], or p11 knockout in NAc ChIs [158] is sufficient to reduce sucrose preference and increase forced-swim immobility (Fig. 2, top).”
From The molecular and cellular mechanisms of depression: a focus on reward circuitry (2019) · cites this paper as [158]
In the citing paper
“Silencing NAc cholinergic interneurons (ChIs) results in anhedonia and increases immobility in the forced-swim and tail-suspension tests [158].”
From The molecular and cellular mechanisms of depression: a focus on reward circuitry (2019) · cites this paper as [158]
In the citing paper
“a recent study has shown that decreasing striatal cholinergic tone in the mouse can lead to depression-like symptoms, likely through interneuron-dependent disinhibition of striatal neurons (Warner-Schmidt et al., 2012)”
From Acetylcholine as a Neuromodulator: Cholinergic Signaling Shapes Nervous System Function and Behavior (2012) · cites this paper as Warner-Schmidt et al., 2012
In the citing paper
“decreasing cholinergic transmission in the striatum can induce depression-like effects in mice through disinhibition of medium spiny neurons (Warner-Schmidt et al., 2012)”
From Mood and anxiety regulation by nicotinic acetylcholine receptors: A potential pathway to modulate aggression and related behavioral states (2015) · cites this paper as Warner-Schmidt et al., 2012
In the citing paper
“numerous studies have now demonstrated that alterations of neuronal activity in the mesolimbic system can result in antidepressant-like effects (Nestler, 2014; Nestler and Carlezon, 2006; Warner-Schmidt et al., 2012)”
From Mood and anxiety regulation by nicotinic acetylcholine receptors: A potential pathway to modulate aggression and related behavioral states (2015) · cites this paper as Warner-Schmidt et al., 2012
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Items 101–163 of 163
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Metadata
- Authors
- Warner-Schmidt, J. L., Schmidt, E. F., Marshall, J. J., Rubin, A. J., Arango-Lievano, M., Kaplitt, M. G., Ibañez-Tallon, I., Heintz, N., & Greengard, P.
- Affiliations
- Laboratories of aMolecular and Cellular Neuroscience and
- Howard Hughes Medical Institute (US)
- Weill Cornell Medicine (US)
- Molecular Biology and Howard Hughes Medical Institute, The Rockefeller University, New York, NY 10065;
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2012-06-25
- Volume
- 109
- Issue
- 28
- Pages
- 11360-11365
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC3396525
- OpenAlex
- W2004051792
- Cited by
- 163
- References
- 37
- Citations by year
- 2026: 6 · 2025: 6 · 2024: 8 · 2023: 11 · 2022: 14 · 2021: 20 · 2020: 11 · 2019: 13 · 2018: 9 · 2017: 14 · 2016: 11 · 2015: 13 · 2014: 11 · 2013: 11 · 2012: 5
- FWCI
- 5.27
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Howard Hughes Medical Institute
- National Institute on Aging (AG09464, P01AG009464)
- National Institute of Mental Health (P50MH090963, MH090963)
- National Institute on Drug Abuse (RC2DA028968)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- cholinergic interneurons, nucleus accumbens, depression-like behavior, p11, major depressive disorder, mood regulation, motivation, neuronal silencing, neural transmission
- MeSH terms
- S100 Calcium Binding Protein A10, Acetylcholine, Animals, Antidepressive Agents, Behavior, Animal, Depression, Immunohistochemistry, Interneurons, Male, Mice, Inbred C57BL, Models, Biological, S100 Proteins, Neurons, Nucleus Accumbens, Phenotype, Receptors, Cholinergic, Annexin A2, Mice, Knockout, Neurotransmitter Agents, Molecular Chaperones, 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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