Evidence map›Paper›PMID 21081162›Full record

ReviewNeurobiology of disease2011

Animal models of dystonia: Lessons from a mutant rat.

Mark S LeDoux

Open access · greenAbstract readReview
In one paragraph

Review in Neurobiology of disease, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.3field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

33 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
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  4. Dystonia in veterinary neurology.Journal of veterinary internal medicine · 2022
    Review
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  7. Review
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  11. 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 · 2017
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Mark S LeDouxUniversity of Tennessee Health Science Center, Department of Neurology, 855 Monroe Avenue, Link Building, Suite 415, Memphis, TN 38163, USA. mledoux@uthsc.edu
University of Tennessee Health Science Center · US

Funding

Dystonia CoalitionU54NS065701 · NINDS · EMORY UNIVERSITY · PI JINNAH, HYDER A · 2009 to 2014
$7.0M
Dystonia CoalitionU54TR001456 · NCATS · EMORY UNIVERSITY · PI JINNAH, HYDER A · 2015 to 2016
$2.5M
The Role of THAP1 in DystoniaR01NS069936 · NINDS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI LEDOUX, MARK S · 2010 to 2013
$1.3M
Mutant Gene Identification in the Dystonic RatR01NS048458 · NINDS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI LEDOUX, MARK S · 2005 to 2008
$800k
Molecular Foundations of the Myoclonus-Dystonia SyndromeR03NS050185 · NINDS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI LEDOUX, MARK S · 2005 to 2006
$144k
CONTROL OF CEREBELLAR OUTPUT IN A DYSTONIA MODELK08NS001593 · NINDS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI LEDOUX, MARK S · 1993 to 1998
–
NCATS NIH HHS U54 TR001456NINDS NIH HHS K08NS001593NINDS NIH HHS R01 NS048458NINDS NIH HHS R01NS048458NINDS NIH HHS R01 NS069936NINDS NIH HHS R01NS069936NINDS NIH HHS R03 NS050185NINDS NIH HHS R03NS050185NINDS NIH HHS U54 NS065701NINDS NIH HHS U54NS065701
6 · The paper itself

Abstract

Dystonia is a motor sign characterized by involuntary muscle contractions which produce abnormal postures. Genetic factors contribute significantly to primary dystonia. In comparison, secondary dystonia can be caused by a wide variety of metabolic, structural, infectious, toxic and inflammatory insults to the nervous system. Although classically ascribed to dysfunction of the basal ganglia, studies of diverse animal models have pointed out that dystonia is a network disorder with important contributions from abnormal olivocerebellar signaling. In particular, work with the dystonic (dt) rat has engendered dramatic paradigm shifts in dystonia research. The dt rat manifests generalized dystonia caused by deficiency of the neuronally restricted protein caytaxin. Electrophysiological and biochemical studies have shown that defects at the climbing fiber-Purkinje cell synapse in the dt rat lead to abnormal bursting firing patterns in the cerebellar nuclei, which increases linearly with postnatal age. In a general sense, the dt rat has shown the scientific and clinical communities that dystonia can arise from dysfunctional cerebellar cortex. Furthermore, work with the dt rat has provided evidence that dystonia (1) is a neurodevelopmental network disorder and (2) can be driven by abnormal cerebellar output. In large part, work with other animal models has expanded upon studies in the dt rat and shown that primary dystonia is a multi-nodal network disorder associated with defective sensorimotor integration. In addition, experiments in genetically engineered models have been used to examine the underlying cellular pathologies that drive primary dystonia. This article is part of a Special Issue entitled "Advances in dystonia".

Indexed as

Disease Models, AnimalAnimalsCerebellumCerebral CortexDystoniaDystonic DisordersMiceRatsRats, Mutant Strains

Identifiers

PMID21081162
PMCPMC3171987
OpenAlexW1997835266

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.