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A New Regulatory Mechanism for Kv7.2 Protein During Neuropathy: Enhanced Transport from the Soma to Axonal Terminals of Injured Sensory Neurons

Overview of attention for article published in Frontiers in Cellular Neuroscience, December 2015
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Title
A New Regulatory Mechanism for Kv7.2 Protein During Neuropathy: Enhanced Transport from the Soma to Axonal Terminals of Injured Sensory Neurons
Published in
Frontiers in Cellular Neuroscience, December 2015
DOI 10.3389/fncel.2015.00470
Pubmed ID
Authors

Elsa Cisneros, Carolina Roza, Nieka Jackson, José Antonio López-García

Abstract

Kv7.2 channel expression has been reported to decrease in dorsal root ganglia (DRG) following the induction of a peripheral neuropathy while other experiments show that Kv7.2 accumulates in peripheral neuromas. The mechanisms underlying these novel expression patterns are poorly understood. Here we use immunofluorescence methods to analyze Kv7.2 protein expression changes in sensory neurons following peripheral axotomy and the potential role of axonal transport. Results indicate that DRG neurons express Kv7.2 in ~16% of neurons and that this number decreases by about 65% after axotomy. Damaged neurons were identified in DRG by application of the tracer Fluoro-ruby at the site of injury during surgery. Reduction of Kv7.2 expression was particularly strong in damaged neurons although some loss was also found in putative uninjured neurons. In parallel to the decrease in the soma of axotomized sensory neurons, Kv7.2 accumulated at neuromatose fiber endings. Blockade of axonal transport with either vinblastine (VLB) or colchicine (COL) abolished Kv7.2 redistribution in neuropathic animals. Channel distribution rearrangements did not occur following induction of inflammation in the hind paw. Behavioral tests indicate that protein rearrangements within sensory afferents are essential to the development of allodynia under neuropathic conditions. These results suggest that axotomy enhances axonal transport in injured sensory neurons, leading to a decrease of somatic expression of Kv7.2 protein and a concomitant accumulation in damaged fiber endings. Localized changes in channel expression patterns under pathological conditions may create novel opportunities for Kv7.2 channel openers to act as analgesics.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 21 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 21 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 6 29%
Student > Doctoral Student 3 14%
Student > Bachelor 3 14%
Student > Master 2 10%
Researcher 2 10%
Other 1 5%
Unknown 4 19%
Readers by discipline Count As %
Neuroscience 5 24%
Medicine and Dentistry 5 24%
Agricultural and Biological Sciences 4 19%
Nursing and Health Professions 1 5%
Psychology 1 5%
Other 0 0%
Unknown 5 24%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 02 December 2015.
All research outputs
#20,297,343
of 22,834,308 outputs
Outputs from Frontiers in Cellular Neuroscience
#3,580
of 4,249 outputs
Outputs of similar age
#324,920
of 387,655 outputs
Outputs of similar age from Frontiers in Cellular Neuroscience
#84
of 99 outputs
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