ArticleBehavioural brain research2015
Decreased dopamine receptor 1 activity and impaired motor-skill transfer in Dyt1 ΔGAG heterozygous knock-in mice.
Article in Behavioural brain research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- Further Studies on the Role of BTBD9 in the Cerebellum, Sleep-like Behaviors and the Restless Legs Syndrome.Neuroscience · 2022Article
- Electrophysiological characterization of the striatal cholinergic interneurons inDystonia (Lausanne, Switzerland) · 2022Article
- Reversal of motor-skill transfer impairment by trihexyphenidyl and reduction of dorsolateral striatal cholinergic interneurons inIBRO neuroscience reports · 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
- A2A Receptor Dysregulation in Dystonia DYT1 Knock-Out Mice.International journal of molecular sciences · 2021Article
- Mu opioid receptor knockout mouse: Phenotypes with implications on restless legs syndrome.Journal of neuroscience research · 2020Article
- BTBD9 and dopaminergic dysfunction in the pathogenesis of restless legs syndrome.Brain structure & function · 2020Article
- Improved survival and overt "dystonic" symptoms in a torsinA hypofunction mouse model.Behavioural brain research · 2020Article
- Decreased number of striatal cholinergic interneurons and motor deficits in dopamine receptor 2-expressing-cell-specific Dyt1 conditional knockout mice.Neurobiology of disease · 2020Article
- Probe the relationship betweenExperimental results · 2020Article
- The role of BTBD9 in the cerebral cortex and the pathogenesis of restless legs syndrome.Experimental neurology · 2020Article
- Hyperactivity, dopaminergic abnormalities, iron deficiency and anemia in an in vivo opioid receptors knockout mouse: Implications for the restless legs syndrome.Behavioural brain research · 2019Article
- Subtle changes in striatal muscarinic M1 and M4 receptor expression in the DYT1 knock-in mouse model of dystonia.PloS one · 2019Article
- 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
- Phosphodiesterase-10A Inverse Changes in Striatopallidal and Striatoentopeduncular Pathways of a Transgenic Mouse Model ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- In vivo imaging reveals impaired connectivity across cortical and subcortical networks in a mouse model of DYT1 dystonia.Neurobiology of disease · 2016Article
- Tor1a+/- mice develop dystonia-like movements via a striatal dopaminergic dysregulation triggered by peripheral nerve injury.Acta neuropathologica communications · 2016Article
- Dopamine receptor and Gα(olf) expression in DYT1 dystonia mouse models during postnatal development.PloS one · 2015Article
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
DYT1 dystonia is a movement disorder caused by a trinucleotide deletion (ΔGAG) in DYT1 (TOR1A), corresponding to a glutamic acid loss in the C-terminal region of torsinA. Functional alterations in the basal ganglia circuits have been reported in both DYT1 dystonia patients and rodent models. Dyt1 ΔGAG heterozygous knock-in (KI) mice exhibit motor deficits and decreased striatal dopamine receptor 2 (D2R) binding activity, suggesting a malfunction of the indirect pathway. However, the role of the direct pathway in pathogenesis of dystonia is not yet clear. Here, we report that Dyt1 KI mice exhibit significantly decreased striatal dopamine receptor 1 (D1R) binding activity and D1R protein levels, suggesting the alteration of the direct pathway. The decreased D1R may be caused by translational or post-translational processes since Dyt1 KI mice had normal levels of striatal D1R mRNA and a normal number of striatal neurons expressing D1R. Levels of striatal ionotropic glutamate receptor subunits, dopamine transporter, acetylcholine muscarinic M4 receptor and adenosine A2A receptor were not altered suggesting a specificity of affected polytopic membrane-associated proteins. Contribution of the direct pathway to motor-skill learning has been suggested in another pharmacological rat model injected with a D1R antagonist. In the present study, we developed a novel motor skill transfer test for mice and found deficits in Dyt1 KI mice. Further characterization of both the direct and the indirect pathways in Dyt1 KI mice will aid the development of novel therapeutic drugs.
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