ArticleBehavioural brain research2012
An anticholinergic reverses motor control and corticostriatal LTD deficits in Dyt1 ΔGAG knock-in mice.
Article in Behavioural brain research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 90 citations in OpenAlex.
- Rescue globus pallidus deep brain stimulation following refractory dystonia treated with subthalamic nucleus deep brain stimulation: illustrative case.Journal of neurosurgery. Case lessons · 2025Article
- Altered Functional Brain Connectivity in Dyt1 Knock-in mouse models.Dystonia (Lausanne, Switzerland) · 2025Article
- Immediate effects of extracorporeal radial pressure wave therapy on dystonia, static plantar pressure distribution, and balance in patients with Parkinson's disease.Frontiers in aging neuroscience · 2025Article
- Behavioral signature of trihexyphenidyl in theDystonia (Lausanne, Switzerland) · 2025Article
- Cell-specific Dyt1 ∆GAG knock-in to basal ganglia and cerebellum reveal differential effects on motor behavior and sensorimotor network function.Experimental neurology · 2023Article
- The muscarinic M4 acetylcholine receptor exacerbates symptoms of movement disorders.Biochemical Society transactions · 2023Review
- Motor deficit and lack of overt dystonia in Dlx conditional Dyt1 knockout mice.Behavioural brain research · 2023Article
- DYT-Frontiers in neuroscience · 2023Review
- Electrophysiological characterization of the striatal cholinergic interneurons inDystonia (Lausanne, Switzerland) · 2022Article
- A dystonia mouse model with motor and sequencing deficits paralleling human disease.Behavioural brain research · 2022Article
- Genetic evidence of aberrant striatal synaptic maturation and secretory pathway alteration in a dystonia mouse model.Dystonia (Lausanne, Switzerland) · 2022Article
- Vesicular Acetylcholine Transporter Alters Cholinergic Tone and Synaptic Plasticity in DYT1 Dystonia.Movement disorders : official journal of the Movement Disorder Society · 2021Article
- 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
- 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
- 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
- CNS critical periods: implications for dystonia and other neurodevelopmental disorders.JCI insight · 2021Review
- The abnormal firing of Purkinje cells in the knockin mouse model of DYT1 dystonia.Brain research bulletin · 2020Article
- BTBD9 and dopaminergic dysfunction in the pathogenesis of restless legs syndrome.Brain structure & function · 2020Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
Abstract
DYT1 early-onset generalized torsion dystonia is an inherited movement disorder associated with mutations in DYT1 that codes for torsinA protein. The most common mutation seen in this gene is a trinucleotide deletion of GAG. We previously reported a motor control deficit on a beam-walking task in our Dyt1 ΔGAG knock-in heterozygous mice. In this report we show the reversal of this motor deficit with the anticholinergic trihexyphenidyl (THP), a drug commonly used to treat movement problems in dystonia patients. THP also restored the reduced corticostriatal long-term depression (LTD) observed in these mice. Corticostriatal LTD has long been known to be dependent on D2 receptor activation. In this mouse model, striatal D2 receptors were expressed at lower quantities in comparison to wild-type mice. Furthermore, the mice were also partially resistant to FPL64176, an agonist of L-type calcium channels that have been previously reported to cause severe dystonic-like symptoms in wild-type mice. Our findings collectively suggest that altered communication between cholinergic interneurons and medium spiny neurons is responsible for the LTD deficit and that this synaptic plasticity modification may be involved in the striatal motor control abnormalities in our mouse model of DYT1 dystonia.
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