ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2022
Nicotinic Acetylcholine Receptors Expressed by Striatal Interneurons Inhibit Striatal Activity and Control Striatal-Dependent Behaviors.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 15 citations in OpenAlex.
- Extrinsic and intrinsic control of striatal cholinergic interneuron activity.Frontiers in molecular neuroscience · 2025Review
- Cholinergic mu-opioid receptor deletion alters reward preference and aversion-resistance.Neuropharmacology · 2024Article
- Effect of chronic vapor nicotine exposure on affective and cognitive behavior in male mice.Scientific reports · 2024Article
- Article
- Cholinergic control of striatal GABAergic microcircuits.Cell reports · 2022Article
- Article
- Synaptic determinants of cholinergic interneurons hyperactivity during parkinsonism.Frontiers in synaptic neuroscience · 2022Article
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Authors and funding
13 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acetylcholine is an important modulator of striatal activity, and it is vital to controlling striatal-dependent behaviors, including motor and cognitive functions. Despite this significance, the mechanisms determining how acetylcholine impacts striatal signaling are still not fully understood. In particular, little is known about the role of nAChRs expressed by striatal interneurons. In the present study, we used FISH to determine which neuronal types express the most prevalent beta2 nicotinic subunit in the mouse striatum. Our data support a common view that nAChR expression is mostly restricted to striatal interneurons. Surprisingly though, cholinergic interneurons were identified as a population with the highest expression of beta2 nicotinic subunit. To investigate the functional significance of beta2-containing nAChRs in striatal interneurons, we deleted them by injecting the AAV-Cre vector into the striatum of
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