ArticleNeurobiology of disease2019
Trihexyphenidyl rescues the deficit in dopamine neurotransmission in a mouse model of DYT1 dystonia.
Article in Neurobiology of disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 39 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
- Trihexyphenidyl Ameliorates Depression-like Behaviors in Adult Zebrafish Exposed to Chronic Unpredictable Stress, Consistent with Regulation of the MAPK Signaling Pathway.Biomolecules · 2026Article
- Article
- Behavioral signature of trihexyphenidyl in theDystonia (Lausanne, Switzerland) · 2025Article
- Neurosurgical and pharmacological management of dystonia.World journal of psychiatry · 2024Review
- A sex-specific effect of MFrontiers in molecular neuroscience · 2024Article
- Trihexyphenidyl Alters Its Host's Metabolism, Neurobehavioral Patterns, and Gut Microbiome Feedback Loop-The Modulating Role ofAntioxidants (Basel, Switzerland) · 2023Article
- Striatal Subregion-selective Dysregulated Dopamine Receptor-mediated Intracellular Signaling in a Model of DOPA-responsive Dystonia.Neuroscience · 2023Article
- Motor deficit and lack of overt dystonia in Dlx conditional Dyt1 knockout mice.Behavioural brain research · 2023Article
- SPARSE: a sparse hypergraph neural network for learning multiple types of latent combinations to accurately predict drug-drug interactions.Bioinformatics (Oxford, England) · 2022Article
- Reversal of motor-skill transfer impairment by trihexyphenidyl and reduction of dorsolateral striatal cholinergic interneurons inIBRO neuroscience reports · 2021Article
- Discovery of the First Selective MACS pharmacology & translational science · 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
- 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
- A Novel Reduced Graphene Oxide Modified Carbon Paste Electrode for Potentiometric Determination of Trihexyphenidyl Hydrochloride in Pharmaceutical and Biological Matrices.Sensors (Basel, Switzerland) · 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
- The Dystonia Coalition: A Multicenter Network for Clinical and Translational Studies.Frontiers in neurology · 2021Review
- Dopamine-receptor blocking agent-associated akathisia: a summary of current understanding and proposal for a rational approach to treatment.Therapeutic advances in psychopharmacology · 2020Review
- The neurobiological basis for novel experimental therapeutics in dystonia.Neurobiology of disease · 2019Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Trihexyphenidyl, a nonselective muscarinic receptor antagonist, is the small molecule drug of choice for the treatment of DYT1 dystonia, but it is poorly tolerated due to significant side effects. A better understanding of the mechanism of action of trihexyphenidyl is needed for the development of improved treatments. Because DTY1 dystonia is associated with both abnormal cholinergic neurotransmission and abnormal dopamine regulation, we tested the hypothesis that trihexyphenidyl normalizes striatal dopamine release in a mouse model of DYT1 dystonia using ex vivo fast scan cyclic voltammetry and in vivo microdialysis. Trihexyphenidyl increased striatal dopamine release and efflux as assessed by ex vivo voltammetry and in vivo microdialysis respectively. In contrast, ʟ-DOPA, which is not usually effective for the treatment of DYT1 dystonia, did not increase dopamine release in either Dyt1 or control mice. Trihexyphenidyl was less effective at enhancing dopamine release in Dyt1 mice relative to controls ex vivo (mean increase WT: 65% vs Dyt1: 35%). Trihexyphenidyl required nicotinic receptors but not glutamate receptors to increase dopamine release. Dyt1 mice were more sensitive to the dopamine release decreasing effects of nicotinic acetylcholine receptor antagonism (IC
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