Evidence map›Paper›PMID 24355600›Full record

ArticleBrain research2014

Redistribution of Kv2.1 ion channels on spinal motoneurons following peripheral nerve injury.

Shannon H Romer, Kathleen M Dominguez, Marc W Gelpi, Adam S Deardorff, Robert C Tracy, Robert E W Fyffe

Abstract read
In one paragraph

Article in Brain research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

22 citing papers in PubMed, 29 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 1 institution in 1 country.

Shannon H RomerDepartment of Neuroscience, Cell Biology and Physiology, 202 University Hall, Wright State University, 3640 Colonel Glenn Hwy, Dayton, OH 45435, USA. Electronic address: Shannon.romer@wright.edu.
Kathleen M DominguezDepartment of Surgery Boonshoft School of Medicine, Wright State University, 3640 Colonel Glenn Hwy, Dayton, OH 45435, USA. Electronic address: Kmdominguez@juno.com.
Marc W GelpiDepartment of Neuroscience, Cell Biology and Physiology, 202 University Hall, Wright State University, 3640 Colonel Glenn Hwy, Dayton, OH 45435, USA. Electronic address: gelpi.2@wright.edu.
Adam S DeardorffDepartment of Neuroscience, Cell Biology and Physiology, 202 University Hall, Wright State University, 3640 Colonel Glenn Hwy, Dayton, OH 45435, USA. Electronic address: deardorff.2@wright.edu.
Robert C TracyDepartment of Neuroscience, Cell Biology and Physiology, 202 University Hall, Wright State University, 3640 Colonel Glenn Hwy, Dayton, OH 45435, USA. Electronic address: robert.tracy@osumc.edu.
Robert E W FyffeDepartment of Neuroscience, Cell Biology and Physiology, 202 University Hall, Wright State University, 3640 Colonel Glenn Hwy, Dayton, OH 45435, USA. Electronic address: robert.fyffe@wright.edu.
Wright State University · US

Funding

Synaptic Function: Effects of the Nerve Injury, Repair, and Altered ActivityP01NS057228 · NINDS · WRIGHT STATE UNIVERSITY · PI COPE, TIMOTHY C · 2007 to 2017
$9.1M
MECHANISMS OF RENSHAW CELL MEDIATED RECURRENT INHIBITIONR01NS025547 · NINDS · WRIGHT STATE UNIVERSITY · PI FYFFE, ROBERT E · 1988 to 2008
$2.3M
NINDS NIH HHS 5P01NS057228NINDS NIH HHS P01 NS057228NINDS NIH HHS R01 NS025547
6 · The paper itself

Abstract

Pathophysiological responses to peripheral nerve injury include alterations in the activity, intrinsic membrane properties and excitability of spinal neurons. The intrinsic excitability of α-motoneurons is controlled in part by the expression, regulation, and distribution of membrane-bound ion channels. Ion channels, such as Kv2.1 and SK, which underlie delayed rectifier potassium currents and afterhyperpolarization respectively, are localized in high-density clusters at specific postsynaptic sites (Deardorff et al., 2013; Muennich and Fyffe, 2004). Previous work has indicated that Kv2.1 channel clustering and kinetics are regulated by a variety of stimuli including ischemia, hypoxia, neuromodulator action and increased activity. Regulation occurs via channel dephosphorylation leading to both declustering and alterations in channel kinetics, thus normalizing activity (Misonou et al., 2004; Misonou et al., 2005; Misonou et al., 2008; Mohapatra et al., 2009; Park et al., 2006). Here we demonstrate using immunohistochemistry that peripheral nerve injury is also sufficient to alter the surface distribution of Kv2.1 channels on motoneurons. The dynamic changes in channel localization include a rapid progressive decline in cluster size, beginning immediately after axotomy, and reaching maximum within one week. With reinnervation, the organization and size of Kv2.1 clusters do not fully recover. However, in the absence of reinnervation Kv2.1 cluster sizes fully recover. Moreover, unilateral peripheral nerve injury evokes parallel, but smaller effects bilaterally. These results suggest that homeostatic regulation of motoneuron Kv2.1 membrane distribution after axon injury is largely independent of axon reinnervation.

Indexed as

AnimalsFemaleMotor NeuronsPeripheral Nerve InjuriesRatsRats, Sprague-DawleyShab Potassium ChannelsTibial NerveKcnb1 protein, ratShab Potassium Channelscholera toxin subunit BCTBimmunoreactivityIRKv2.1lateral gastrocnemius muscleLGmedial gastrocnemius muscleMGMNmotoneuronMotoneuronperipheral Nerve InjuryPeripheral nerve injuryPNIVoltage-gated ion channels

Identifiers

PMID24355600
PMCPMC3970712
OpenAlexW2080657366

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.