Evidence map›Paper›PMID 20410108›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010

Evidence from computer simulations for alterations in the membrane biophysical properties and dendritic processing of synaptic inputs in mutant superoxide dismutase-1 motoneurons.

Sherif M Elbasiouny, Julien Amendola, Jacques Durand, C J Heckman

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 2 pooled it
2.6field-weighted citation impact, top 11% 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

23 citing papers in PubMed, 2 syntheses or guidelines pooled it, 46 citations in OpenAlex.

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  14. Development of modified cable models to simulate accurate neuronal active behaviors.Journal of applied physiology (Bethesda, Md. : 1985) · 2014
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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

4 authors at 2 institutions in 2 countries.

Sherif M ElbasiounyDepartment of Physiology, Northwestern University, Chicago, Illinois 60611, USA. s-lbasiouny@northwestern.edu
Julien Amendola
Jacques Durand
C J Heckman
Institut de Neurobiologie de la Méditerranée · FRNorthwestern University · US

Funding

Increased persistent sodium current in SOD1 motoneuronsR01NS051462 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI HECKMAN, CHARLES · 2005 to 2009
$1.6M
CIHRNINDS NIH HHS NS051462NINDS NIH HHS R01 NS051462
6 · The paper itself

Abstract

A critical step in improving our understanding of the development of amyotrophic lateral sclerosis (ALS) is to identify the factors contributing to the alterations in the excitability of motoneurons and assess their individual contributions. Here we investigated the early alterations in the passive electrical and morphological properties of neonatal spinal motoneurons that occur by 10 d after birth, long before disease onset. We identified some of the factors contributing to these alterations, and estimated their individual contributions. To achieve this goal, we undertook a computer simulation analysis using realistic morphologies of reconstructed wild-type (WT) and mutant superoxide dismutase-1 (mSOD1) motoneurons. Ion channel parameters of these models were then tuned to match the experimental data on electrical properties obtained from these same motoneurons. We found that the reduced excitability of mSOD1 models was accompanied with decreased specific membrane resistance by approximately 25% and efficacy of synaptic inputs (slow and fast) by 12-22%. Linearity of summation of synaptic currents was similar to WT. We also assessed the contribution of the alteration in dendritic morphology alone to this decreased excitability and found that it reduced the input resistance by 10% and the efficacy of synaptic inputs by 7-15%. Our results were also confirmed in models with dendritic active conductances. Our simulations indicated that the alteration in passive electrical properties of mSOD1 models resulted from concurrent alterations in their morphology and membrane biophysical properties, and consequently altered the motoneuronal dendritic processing of synaptic inputs. These results clarify new aspects of spinal motoneurons malfunction in ALS.

Indexed as

Computer SimulationAnimalsCell MembraneDendritesExcitatory Postsynaptic PotentialsMiceMice, TransgenicMotor NeuronsMutationNeural InhibitionSuperoxide DismutaseSuperoxide Dismutase-1SynapsesSod1 protein, mouseSuperoxide DismutaseSuperoxide Dismutase-1

Identifiers

PMID20410108
PMCPMC4671367
OpenAlexW2047066220

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.