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Specific ion channels contribute to key elements of pathology during secondary degeneration following neurotrauma

Overview of attention for article published in BMC Neuroscience, August 2017
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Title
Specific ion channels contribute to key elements of pathology during secondary degeneration following neurotrauma
Published in
BMC Neuroscience, August 2017
DOI 10.1186/s12868-017-0380-1
Pubmed ID
Authors

Ryan L. O’Hare Doig, Wissam Chiha, Marcus K. Giacci, Nathanael J. Yates, Carole A. Bartlett, Nicole M. Smith, Stuart I. Hodgetts, Alan R. Harvey, Melinda Fitzgerald

Abstract

Following partial injury to the central nervous system, cells beyond the initial injury site undergo secondary degeneration, exacerbating loss of neurons, compact myelin and function. Changes in Ca(2+) flux are associated with metabolic and structural changes, but it is not yet clear how flux through specific ion channels contributes to the various pathologies. Here, partial optic nerve transection in adult female rats was used to model secondary degeneration. Treatment with combinations of three ion channel inhibitors was used as a tool to investigate which elements of oxidative and structural damage related to long term functional outcomes. The inhibitors employed were the voltage gated Ca(2+) channel inhibitor Lomerizine (Lom), the Ca(2+) permeable AMPA receptor inhibitor YM872 and the P2X7 receptor inhibitor oxATP. Following partial optic nerve transection, hyper-phosphorylation of Tau and acetylated tubulin immunoreactivity were increased, and Nogo-A immunoreactivity was decreased, indicating that axonal changes occurred acutely. All combinations of ion channel inhibitors reduced hyper-phosphorylation of Tau and increased Nogo-A immunoreactivity at day 3 after injury. However, only Lom/oxATP or all three inhibitors in combination significantly reduced acetylated tubulin immunoreactivity. Most combinations of ion channel inhibitors were effective in restoring the lengths of the paranode and the paranodal gap, indicative of the length of the node of Ranvier, following injury. However, only all three inhibitors in combination restored to normal Ankyrin G length at the node of Ranvier. Similarly, HNE immunoreactivity and loss of oligodendrocyte precursor cells were only limited by treatment with all three ion channel inhibitors in combination. Data indicate that inhibiting any of a range of ion channels preserves certain elements of axon and node structure and limits some oxidative damage following injury, whereas ionic flux through all three channels must be inhibited to prevent lipid peroxidation and preserve Ankyrin G distribution and OPCs.

Twitter Demographics

The data shown below were collected from the profile of 1 tweeter who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 37 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 37 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 9 24%
Researcher 7 19%
Student > Master 6 16%
Student > Doctoral Student 2 5%
Student > Bachelor 2 5%
Other 3 8%
Unknown 8 22%
Readers by discipline Count As %
Neuroscience 12 32%
Medicine and Dentistry 4 11%
Biochemistry, Genetics and Molecular Biology 3 8%
Psychology 3 8%
Veterinary Science and Veterinary Medicine 2 5%
Other 3 8%
Unknown 10 27%

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 14 August 2017.
All research outputs
#10,297,625
of 11,609,687 outputs
Outputs from BMC Neuroscience
#797
of 954 outputs
Outputs of similar age
#223,803
of 264,826 outputs
Outputs of similar age from BMC Neuroscience
#18
of 20 outputs
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