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GENERAL COMMENTARY article

Front. Integr. Neurosci., 16 June 2014
Volume 8 - 2014 | https://doi.org/10.3389/fnint.2014.00049
This article is part of the Research Topic Mechanisms of Motor Function Recovery after Spinal Cord Injury View all 12 articles

Corrigendum: Recovery of neuronal and network excitability after spinal cord injury and implications for spasticity

This article is a commentary on:

  1. Recovery of neuronal and network excitability after spinal cord injury and implications for spasticity

    1. Read original article
\r\nJessica M. D&#x;Amico,Jessica M. D'Amico1,2Elizabeth G. Condliffe,,,Elizabeth G. Condliffe1,2,3,4Karen J. B. Martins,Karen J. B. Martins1,5David J. Bennett,David J. Bennett1,6Monica A. Gorassini,,*Monica A. Gorassini1,2,3*
  • 1Centre for Neuroscience, University of Alberta, Edmonton, AB, Canada
  • 2Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB, Canada
  • 3Department of Biomedical Engineering, University of Alberta, Edmonton, AB, Canada
  • 4Division of Physical Medicine and Rehabilitation, University of Alberta, Edmonton, AB, Canada
  • 5Faculty of Physical Education and Recreation, University of Alberta, Edmonton, AB, Canada
  • 6Faculty of Rehabilitation Medicine, University of Alberta, Edmonton, AB, Canada

A corrigendum on
Recovery of neuronal and network excitability after spinal cord injury and implications for spasticity

by D'Amico, J. M., Condliffe, E. G., Martins, K. J. B., Bennett, D. J., and Gorassini, M. A. (2014). Front. Integr. Neurosci. 8:36. doi: 10.3389/fnint.2014.00036

In Figure 10 of D'Amico et al. (2014) the KCC2 co-transporter was incorrectly drawn as a co-exchanger. This has been corrected in this version of the figure to show that both chloride and potassium are pumped out of the motoneuron.

FIGURE 10
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Figure 10. KCC2 cotransporter and chloride equilibrium before and after SCI. (A) A potassium chloride cotransporter (KCC2) transports both chloride (Cl−) and potassium (K+) out of the motoneuron (MN) to maintain Cl− equilibrium potential below resting membrane potential, allowing Cl− influx and MN hyperpolarization during activation of GABA and Glycine receptors (R). (B) Downregulation of KCC2 expression in motoneurons after SCI increases intracellular Cl− concentration, depolarizing Cl− equilibrium potential to above rest. This produces efflux of Cl− and depolarization of MN during activation of GABA and Glycine receptors. Activation of 5-HT2A receptors increases cell membrane expression of KCC2 after SCI to restore endogenous inhibition.

Conflict of Interest Statement

The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Keywords: spasticity, motoneurons, spinal cord injury, rehabilitation, reflex

Citation: D'Amico JM, Condliffe EG, Martins KJB, Bennett DJ and Gorassini MA (2014) Corrigendum: Recovery of neuronal and network excitability after spinal cord injury and implications for spasticity. Front. Integr. Neurosci. 8:49. doi: 10.3389/fnint.2014.00049

Received: 22 May 2014; Accepted: 26 May 2014;
Published online: 16 June 2014.

Edited by:

Martin Oudega, University of Pittsburgh, USA

Reviewed by:

Robert M. Brownstone, Dalhousie University, Canada

Copyright © 2014 D'Amico, Condliffe, Martins, Bennett and Gorassini. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: monica.gorassini@ualberta.ca

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