Front. Integr. Neurosci. Frontiers in Integrative Neuroscience Front. Integr. Neurosci. 1662-5145 Frontiers Media S.A. 10.3389/fnint.2014.00049 Neuroscience General Commentary Article Corrigendum: Recovery of neuronal and network excitability after spinal cord injury and implications for spasticity D'Amico Jessica M. 1 2 Condliffe Elizabeth G. 1 2 3 4 Martins Karen J. B. 1 5 Bennett David J. 1 6 Gorassini Monica A. 1 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

*Correspondence: monica.gorassini@ualberta.ca

Edited by: Martin Oudega, University of Pittsburgh, USA

Reviewed by: Robert M. Brownstone, Dalhousie University, Canada

This article was submitted to the journal Frontiers in Integrative Neuroscience.

 16 06 2014 2014 8 49 22 05 2014 26 05 2014 Copyright © 2014 D'Amico, Condliffe, Martins, Bennett and Gorassini. 2014

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 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 spasticity motoneurons spinal cord injury rehabilitation reflex

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.

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.