Evidence map›Paper›PMID 21177993›Full record

ArticleJournal of neurophysiology2011

Alterations of action potentials and the localization of Nav1.6 sodium channels in spared axons after hemisection injury of the spinal cord in adult rats.

Arsen S Hunanyan, Valentina Alessi, Samik Patel, Damien D Pearse, Gary Matthews, Victor L Arvanian

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neurophysiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 32 citations in OpenAlex.

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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

6 authors at 4 institutions in 1 country.

Arsen S HunanyanNorthport Veterans Affairs Medical Center, 79 Middleville Road, Bld. 62, Northport, NY 11768, USA.
Valentina Alessi
Samik Patel
Damien D Pearse
Gary Matthews
Victor L Arvanian
Neurological Surgery · USNorthport VA Medical Center · USState University of New York · USStony Brook University · US

Funding

CELLULAR NEUROPHYSIOLOGY OF THE VERTEBRATE RETINAR01EY003821 · NEI · STATE UNIVERSITY NEW YORK STONY BROOK · PI WOLLMUTH, LONNIE P · 1985 to 2019
$8.1M
Axon Regenration: Synergistic Actions of the MAPK and Cyclic AMP PathwaysR01NS056281 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI PEARSE, DAMIEN D. · 2007 to 2010
$1.3M
NEI NIH HHS R01 EY003821NINDS NIH HHS R01 NS056281
6 · The paper itself

Abstract

Previously, we reported a pronounced reduction in transmission through surviving axons contralateral to chronic hemisection (HX) of adult rat spinal cord. To examine the cellular and molecular mechanisms responsible for this diminished transmission, we recorded intracellularly from lumbar lateral white matter axons in deeply anesthetized adult rats in vivo and measured the propagation of action potentials (APs) through rubrospinal/reticulospinal tract (RST/RtST) axons contralateral to chronic HX at T10. We found decreased excitability in these axons, manifested by an increased rheobase to trigger APs and longer latency for AP propagation passing the injury level, without significant differences in axonal resting membrane potential and input resistance. These electrophysiological changes were associated with altered spatial localization of Nav1.6 sodium channels along axons: a subset of axons contralateral to the injury exhibited a diffuse localization (>10 μm spread) of Nav1.6 channels, a pattern characteristic of demyelinated axons (Craner MJ, Newcombe J, Black JA, Hartle C, Cuzner ML, Waxman SG. Proc Natl Acad Sci USA 101: 8168-8173, 2004b). This result was substantiated by ultrastructural changes seen with electron microscopy, in which an increased number of large-caliber, demyelinated RST axons were found contralateral to the chronic HX. Therefore, an increased rheobase, pathological changes in the distribution of Nav1.6 sodium channels, and the demyelination of contralateral RST axons are likely responsible for their decreased conduction chronically after HX and thus may provide novel targets for strategies to improve function following incomplete spinal cord injury.

Indexed as

Action PotentialsAnimalsAxonsCells, CulturedFemaleHemiplegiaNAV1.6 Voltage-Gated Sodium ChannelRatsRats, Sprague-DawleySodium ChannelsSpinal CordSpinal Cord InjuriesTissue DistributionNAV1.6 Voltage-Gated Sodium ChannelScn8a protein, ratSodium Channels

Identifiers

PMID21177993
PMCPMC3074424
OpenAlexW2147196321

What OpenQuestion holds

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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.