Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

A Novel Transgenic Mouse Model to Investigate the Cell-Autonomous Effects of torsinA(ΔE) Expression in Striatal Output Neurons.

Neuroscience - 1 Dec 2019

Gonzalez-Alegre Pedro, Beauvais Genevieve, Martin Janine, Koch Rick J, Walker Ruth H, Patel Jyoti C, Rice Margaret E, Ehrlich Michelle E

Abstract excerpt

Dystonia is a disabling neurological syndrome characterized by abnormal movements and postures that result from intermittent or sustained involuntary muscle contractions; mutations of DYT1/TOR1A are the most common cause of childhood-onset, generalized, inherited dystonia. Patient and mouse model data strongly support dysregulation of the nigrostriatal dopamine neurotransmission circuit in the presence of the...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cocaine
Share to Corpus Striatum

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Dopamine

Share to Dystonia

Share to Electric Stimulation

Share to Motor Skills

Share to Neural Pathways

Share to Substantia Nigra

Source

Identifiers

PMID: 31669362
DOI: 10.1016/j.neuroscience.2019.09.007

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A Novel Transgenic Mouse Model to Investigate the Cell-Autonomous Effects of torsinA(ΔE) Expression in Striatal Output Neurons.PMID 31669362Read ↗

Cholinergic dysregulation produced by selective inactivation of the dystonia-associated protein torsinA.Semantic proximity Read ↗

Transgenic mouse model of early-onset DYT1 dystoniaSemantic proximity Read ↗

Motor deficits and decreased striatal dopamine receptor 2 binding activity in the striatum-specific Dyt1 conditional knockout mice.Semantic proximity Read ↗

Cell-intrinsic effects of TorsinA(ΔE) disrupt dopamine release in a mouse model of TOR1A dystonia.Semantic proximity Read ↗

Motor deficits and hyperactivity in Dyt1 knockdown mice.Semantic proximity Read ↗

Dopamine release is impaired in a mouse model of DYT1 dystonia.Semantic proximity Read ↗

Gene expression changes in a transgenic mouse model overexpressing human wildtype and mutant torsinA.Semantic proximity Read ↗

Developmental profile of the aberrant dopamine D2 receptor response in striatal cholinergic interneurons in DYT1 dystonia.Semantic proximity Read ↗

A new knock-in mouse model of l-DOPA-responsive dystonia.Semantic proximity Read ↗

Cell-autonomous alteration of dopaminergic transmission by wild type and mutant (ΔE) TorsinA in transgenic miceSemantic proximity Read ↗

A novel conditional knock-in approach defines molecular and circuit effects of the DYT1 dystonia mutation.Semantic proximity Read ↗

Regional specificity of synaptic plasticity deficits in a knock-in mouse model of DYT1 dystonia.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.