ArticleNeurobiology of disease2010
Cell-autonomous alteration of dopaminergic transmission by wild type and mutant (DeltaE) TorsinA in transgenic mice.
Article in Neurobiology of disease, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 72 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
- Cerebellar contributions to dystonia: unraveling the role of Purkinje cells and cerebellar nuclei.Dystonia (Lausanne, Switzerland) · 2025Article
- Behavioral signature of trihexyphenidyl in theDystonia (Lausanne, Switzerland) · 2025Article
- Motor deficit and lack of overt dystonia in Dlx conditional Dyt1 knockout mice.Behavioural brain research · 2023Article
- DYT-Frontiers in neuroscience · 2023Review
- Characterization of the direct pathway in Dyt1 ΔGAG heterozygous knock-in mice and dopamine receptor 1-expressing-cell-specific Dyt1 conditional knockout mice.Behavioural brain research · 2021Article
- Cell-intrinsic effects of TorsinA(ΔE) disrupt dopamine release in a mouse model of TOR1A dystonia.Neurobiology of disease · 2021Article
- Alteration of the cholinergic system and motor deficits in cholinergic neuron-specific Dyt1 knockout mice.Neurobiology of disease · 2021Article
- Investigating the role of striatal dopamine receptor 2 in motor coordination and balance: Insights into the pathogenesis of DYT1 dystonia.Behavioural brain research · 2021Article
- Decreased number of striatal cholinergic interneurons and motor deficits in dopamine receptor 2-expressing-cell-specific Dyt1 conditional knockout mice.Neurobiology of disease · 2020Article
- Trihexyphenidyl rescues the deficit in dopamine neurotransmission in a mouse model of DYT1 dystonia.Neurobiology of disease · 2019Article
- Postsynaptic movement disorders: clinical phenotypes, genotypes, and disease mechanisms.Journal of inherited metabolic disease · 2018Review
- Dopamine Receptor Agonist Treatment of Idiopathic Dystonia: A Reappraisal in Humans and Mice.The Journal of pharmacology and experimental therapeutics · 2018Article
- Heterozygous Gnal Mice Are a Novel Animal Model with Which to Study Dystonia Pathophysiology.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Article
- The Anatomical Basis for Dystonia: The Motor Network Model.Tremor and other hyperkinetic movements (New York, N.Y.) · 2017Review
- Drosophila Torsin Protein Regulates Motor Control and Stress Sensitivity and Forms a Complex with Fragile-X Mental Retardation Protein.Neural plasticity · 2016Article
- Abnormalities of motor function, transcription and cerebellar structure in mouse models of THAP1 dystonia.Human molecular genetics · 2015Article
- A novel conditional knock-in approach defines molecular and circuit effects of the DYT1 dystonia mutation.Human molecular genetics · 2015Article
- Striatal cholinergic dysfunction as a unifying theme in the pathophysiology of dystonia.Progress in neurobiology · 2015Review
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
Abstract
Early onset torsion dystonia is an autosomal dominant movement disorder of variable penetrance caused by a glutamic acid, i.e. DeltaE, deletion in DYT1, encoding the protein TorsinA. Genetic and structural data implicate basal ganglia dysfunction in dystonia. TorsinA, however, is diffusely expressed, and therefore the primary source of dysfunction may be obscured in pan-neuronal transgenic mouse models. We utilized the tyrosine hydroxylase (TH) promoter to direct transgene expression specifically to dopaminergic neurons of the midbrain to identify cell-autonomous abnormalities. Expression of both the human wild type (hTorsinA) and mutant (DeltaE-hTorsinA) protein resulted in alterations of dopamine release as detected by microdialysis and fast cycle voltammetry. Motor abnormalities detected in these mice mimicked those noted in transgenic mice with pan-neuronal transgene expression. The locomotor response to cocaine in both TH-hTorsinA and TH-DeltaE-hTorsinA, in the face of abnormal extracellular DA levels relative to non-transgenic mice, suggests compensatory, post-synaptic alterations in striatal DA transmission. This is the first cell-subtype-specific DYT1 transgenic mouse that can serve to differentiate between primary and secondary changes in dystonia, thereby helping to target disease therapies.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.