Evidence map›Paper›PMID 21315257›Full record

ArticleNeuron2011

Early functional impairment of sensory-motor connectivity in a mouse model of spinal muscular atrophy.

George Z Mentis, Dvir Blivis, Wenfang Liu, Estelle Drobac, Melissa E Crowder, Lingling Kong, Francisco J Alvarez, Charlotte J Sumner, Michael J O'Donovan

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Neuron, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 244 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
244citing papers in PubMed, 1 pooled it
15.2field-weighted citation impact, top 1% 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

244 citing papers in PubMed, 1 synthesis or guideline pooled it, 385 citations in OpenAlex.

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184 more citing papers are in PubMed but not listed here.

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

9 authors at 5 institutions in 1 country.

George Z MentisSection on Developmental Biology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA. gzmentis@columbia.edu
Dvir Blivis
Wenfang Liu
Estelle Drobac
Melissa E Crowder
Lingling Kong
Francisco J Alvarez
Charlotte J Sumner
Michael J O'Donovan
National Institutes of Health · USJohns Hopkins University · USNational Institute of Neurological Disorders and Stroke · USColumbia University · USWright State University · US

Funding

DEVELOPMENT OF SYNAPTIC INPUTS ON SPINAL INTERNEURONSR01NS047357 · NINDS · WRIGHT STATE UNIVERSITY · PI ALVAREZ, FRANCISCO J · 2004 to 2025
$6.4M
Cellular and Synaptic Organization of the Spinal CordZIANS002787 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI O'DONOVAN, MICHAEL · 2009 to 2013
$4.1M
Muscle and neuromuscular junctions in spinal muscular atrophyR01NS062869 · NINDS · JOHNS HOPKINS UNIVERSITY · PI SUMNER, CHARLOTTE JANE · 2009 to 2013
$1.7M
Howard Hughes Medical InstituteIntramural NIH HHS Z99 NS999999NINDS NIH HHS R01 NS047357NINDS NIH HHS R01 NS062869NINDS NIH HHS R01NS062869
6 · The paper itself

Abstract

To define alterations of neuronal connectivity that occur during motor neuron degeneration, we characterized the function and structure of spinal circuitry in spinal muscular atrophy (SMA) model mice. SMA motor neurons show reduced proprioceptive reflexes that correlate with decreased number and function of synapses on motor neuron somata and proximal dendrites. These abnormalities occur at an early stage of disease in motor neurons innervating proximal hindlimb muscles and medial motor neurons innervating axial muscles, but only at end-stage disease in motor neurons innervating distal hindlimb muscles. Motor neuron loss follows afferent synapse loss with the same temporal and topographical pattern. Trichostatin A, which improves motor behavior and survival of SMA mice, partially restores spinal reflexes, illustrating the reversibility of these synaptic defects. Deafferentation of motor neurons is an early event in SMA and may be a primary cause of motor dysfunction that is amenable to therapeutic intervention.

Indexed as

Disease Models, AnimalAge FactorsAnimalsAnimals, NewbornMiceMice, TransgenicMotor NeuronsMuscular Atrophy, SpinalSensory Receptor CellsSynapses

Identifiers

PMID21315257
PMCPMC3044334
OpenAlexW2101970831

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.