Evidence map›Paper›PMID 29614705›Full record

ArticleRestorative neurology and neuroscience2018

Identification of a resilient mouse facial motoneuron population following target disconnection by injury or disease.

Deborah O Setter, Melissa M Haulcomb, Taylor Beahrs, Rena M Meadows, Nicole D Schartz, Sara K Custer, Virginia M Sanders, Kathryn J Jones

Abstract read
In one paragraph

Article in Restorative neurology and neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 49% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Review
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

8 authors at 5 institutions in 1 country.

Deborah O SetterDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
Melissa M HaulcombDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
Taylor BeahrsDepartment of Cell Biology, Neurobiology, and Anatomy, Loyola University Medical Center, Maywood, IL, USA.
Rena M MeadowsDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
Nicole D SchartzDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
Sara K CusterDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
Virginia M SandersDepartment of Cancer Biology and Genetics, The Ohio State University, Columbus, OH, USA.
Kathryn J JonesDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
Richard L. Roudebush VA Medical Center · USIndiana University – Purdue University Indianapolis · USEdward Hines, Jr. VA Hospital · USIndiana University School of MedicineThe Ohio State University · US

Funding

Immune Regulation of Neuronal Injury and RepairR01NS040433 · NINDS · LOYOLA UNIVERSITY CHICAGO · PI JONES, KATHRYN JANE · 2001 to 2017
$5.9M
NINDS NIH HHS R01 NS040433
6 · The paper itself

Abstract

backgroundWhen nerve transection is performed on adult rodents, a substantial population of neurons survives short-term disconnection from target, and the immune system supports this neuronal survival, however long-term survival remains unknown. Understanding the effects of permanent axotomy on cell body survival is important as target disconnection is the first pathological occurrence in fatal motoneuron diseases such as amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA).

objectiveThe goal of this study was to determine if facial motoneurons (FMN) could survive permanent target disconnection up to 26 weeks post-operation (wpo) after facial nerve axotomy (FNA). In addition, the potentially additive effects of immunodeficiency and motoneuron disease on post-axotomy FMN survival were examined.

methodsThis study included three wild type (WT) mouse strains (C57BL/6J, B6SJL, and FVB/NJ) and three experimental models (RAG-2-/-: immunodeficiency; mSOD1: ALS; Smn-/-/SMN2+/+: SMA). All animals received a unilateral FNA, and FMN survival was quantified at early and extended post-operative timepoints.

resultsIn the C57BL/6J WT group, FMN survival significantly decreased at 10 wpo (55±6%), and then remained stable out to 26 wpo (47±6%). In the RAG-2-/- and mSOD1 groups, FMN death occurred much earlier at 4 wpo, and survival plateaued at approximately 50% at 10 wpo. The SMA model and other WT strains also exhibited approximately 50% FMN survival after FNA.

conclusionThese results indicate that immunodeficiency and motoneuron disease accelerate axotomy-induced neuron death, but do not increase total neuron death in the context of permanent target disconnection. This consistent finding of a target disconnection-resilient motoneuron population is prevalent in other peripheral nerve injury models and in neurodegenerative disease models as well. Characterization of the distinct populations of vulnerable and resilient motoneurons may reveal new therapeutic approaches for injury and disease.

Indexed as

AnimalsAxotomyCell DeathCell SurvivalCentral Nervous System DiseasesFacial NerveFacial Nerve InjuriesMice, Inbred C57BLMotor Neuronsamyotrophic lateral sclerosisaxotomyMotoneuronmotor neuronneuron survivalperipheral nerve injuryspinal muscular atrophy

Identifiers

PMID29614705
PMCPMC6373730
OpenAlexW2794982277

What OpenQuestion holds

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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.