ArticleNeurobiology of disease2021
Cell-intrinsic effects of TorsinA(ΔE) disrupt dopamine release in a mouse model of TOR1A dystonia.
Article in Neurobiology of disease, 2021. 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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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- Optogenetic Inhibition of Striatal Parvalbuminergic Interneurons Unmasks Impaired GABA and Adenosine Signaling in DYT1 Knock-In Mice.International journal of molecular sciences · 2026Article
- Patient-centered brain transcriptomic and multimodal imaging determinants of clinical progression, physical activity, and treatment needs in Parkinson's disease.NPJ Parkinson's disease · 2025Article
- Behavioral signature of trihexyphenidyl in theDystonia (Lausanne, Switzerland) · 2025Article
- eIF2α phosphorylation evokes dystonia-like movements with D2-receptor and cholinergic origin and abnormal neuronal connectivity.bioRxiv : the preprint server for biology · 2024Article
- DYT-Frontiers in neuroscience · 2023Review
- Synaptic Dysfunction in Dystonia: Update From Experimental Models.Current neuropharmacology · 2023Review
- Transgenic Mice for the Translational Study of Neuropathic Pain and Dystonia.International journal of molecular sciences · 2022Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
TOR1A-associated dystonia, otherwise known as DYT1 dystonia, is an inherited dystonia caused by a three base-pair deletion in the TOR1A gene (TOR1AΔE). Although the mechanisms underlying the dystonic movements are largely unknown, abnormalities in striatal dopamine and acetylcholine neurotransmission are consistently implicated whereby dopamine release is reduced while cholinergic tone is increased. Because striatal cholinergic neurotransmission mediates dopamine release, it is not known if the dopamine release deficit is mediated indirectly by abnormal acetylcholine neurotransmission or if Tor1a(ΔE) acts directly within dopaminergic neurons to attenuate release. To dissect the microcircuit that governs the deficit in dopamine release, we conditionally expressed Tor1a(ΔE) in either dopamine neurons or cholinergic interneurons in mice and assessed striatal dopamine release using ex vivo fast scan cyclic voltammetry or dopamine efflux using in vivo microdialysis. Conditional expression of Tor1a(ΔE) in cholinergic neurons did not affect striatal dopamine release. In contrast, conditional expression of Tor1a(ΔE) in dopamine neurons reduced dopamine release to 50% of normal, which is comparable to the deficit in Tor1a
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Registered trials
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