ArticleeLife2018
A cell autonomous torsinA requirement for cholinergic neuron survival and motor control.
Article in eLife, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Altered striosome-matrix distribution and activity of striatal cholinergic interneurons in a model of autism-linked repetitive behaviors.Molecular psychiatry · 2026Article
- Subtle changes in Purkinje cell firing in Purkinje cell-specificDystonia (Lausanne, Switzerland) · 2025Article
- Anticholinergic drugs for parkinsonism and other movement disorders.Journal of neural transmission (Vienna, Austria : 1996) · 2024Review
- A mismatch between striatal cholinergic pauses and dopaminergic reward prediction errors.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Sensory-motor circuit is a therapeutic target forScience advances · 2024Article
- Pathophysiology of Dyt1-Science translational medicine · 2023Article
- Motor deficit and lack of overt dystonia in Dlx conditional Dyt1 knockout mice.Behavioural brain research · 2023Article
- DYT-Frontiers in neuroscience · 2023Review
- Three-Dimensional Spatial Analyses of Cholinergic Neuronal Distributions Across The Mouse Septum, Nucleus Basalis, Globus Pallidus, Nucleus Accumbens, and Caudate-Putamen.Neuroinformatics · 2022Article
- Oligodendrocyte and Extracellular Matrix Contributions to Central Nervous System Motor Function: Implications for Dystonia.Movement disorders : official journal of the Movement Disorder Society · 2022Review
- Collagen VI Regulates Motor Circuit Plasticity and Motor Performance by Cannabinoid Modulation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Reversal of motor-skill transfer impairment by trihexyphenidyl and reduction of dorsolateral striatal cholinergic interneurons inIBRO neuroscience reports · 2021Article
- Cell-specific effects of Dyt1 knock-out on sensory processing, network-level connectivity, and motor deficits.Experimental neurology · 2021Article
- The HIV protease inhibitor, ritonavir, corrects diverse brain phenotypes across development in mouse model of DYT-TOR1A dystonia.Science translational medicine · 2021Article
- Alteration of the cholinergic system and motor deficits in cholinergic neuron-specific Dyt1 knockout mice.Neurobiology of disease · 2021Article
- Cell-intrinsic effects of TorsinA(ΔE) disrupt dopamine release in a mouse model of TOR1A dystonia.Neurobiology of disease · 2021Article
- TorsinA restoration in a mouse model identifies a critical therapeutic window for DYT1 dystonia.The Journal of clinical investigation · 2021Article
- CNS critical periods: implications for dystonia and other neurodevelopmental disorders.JCI insight · 2021Review
- Article
- Decreased number of striatal cholinergic interneurons and motor deficits in dopamine receptor 2-expressing-cell-specific Dyt1 conditional knockout mice.Neurobiology of disease · 2020Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Cholinergic dysfunction is strongly implicated in dystonia pathophysiology. Previously (Pappas et al., 2015;4:e08352), we reported that Dlx5/6-Cre mediated forebrain deletion of the DYT1 dystonia protein torsinA (Dlx-CKO) causes abnormal twisting and selective degeneration of dorsal striatal cholinergic interneurons (ChI) (Pappas et al., 2015). A central question raised by that work is whether the ChI loss is cell autonomous or requires torsinA loss from neurons synaptically connected to ChIs. Here, we addressed this question by using ChAT-Cre mice to conditionally delete torsinA from cholinergic neurons ('ChAT-CKO'). ChAT-CKO mice phenocopy the Dlx-CKO phenotype of selective dorsal striatal ChI loss and identify an essential requirement for torsinA in brainstem and spinal cholinergic neurons. ChAT-CKO mice are tremulous, weak, and exhibit trunk twisting and postural abnormalities. These findings are the first to demonstrate a cell autonomous requirement for torsinA in specific populations of cholinergic neurons, strengthening the connection between torsinA, cholinergic dysfunction and dystonia pathophysiology.
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Registered trials
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