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Brain Advance Access originally published online on August 12, 2008
Brain 2008 131(11):3062-3071; doi:10.1093/brain/awn180
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© The Author (2008). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Up-regulation of slow K+ channels in peripheral motor axons: a transcriptional channelopathy in multiple sclerosis

Karl Ng, James Howells, John D. Pollard and David Burke

Institute of Clinical Neurosciences, Royal Prince Alfred Hospital and The University of Sydney, Sydney, NSW 2006, Australia

Correspondence to: Karl Ng, MRCP, FRACP, Office of Research & Development, Medical Foundation Building – K25, University of Sydney, NSW 2006, Australia E-mail: kng{at}med.usyd.edu.au

Spinal lesions produce plastic changes in motoneuron properties. We have documented the excitability of motor axons in the median nerve of 12 patients with multiple sclerosis and 50 normal subjects, hypothesizing that plastic changes in the properties of spinal motoneurons might be reflected in the properties of peripheral motor axons and be demonstrable in vivo. In the patients, there were changes in physiological measures of axonal excitability attributable to increased slow K+ channel activity. Other measures were within control limits. These changes could be modelled by an 11% increase in slow K+ current, with compensatory changes in membrane potential, suggesting increased expression of the responsible channels. The changes cannot be explained solely by changes in membrane potential and are not those expected if peripheral nerve axons were involved in the inflammatory process of multiple sclerosis. They probably represent a transcriptional channelopathy, due to up-regulation of channel expression. The abnormalities do not imply that peripheral nerve function has been significantly compromised, but they do suggest that the properties of the parent motoneurons have changed. This study thus provides evidence for plasticity in motoneuronal properties at a molecular level, the first such evidence for intact human subjects.

Key Words: slow K channel; multiple sclerosis; motoneuron; channelopathy; plasticity

Abbreviations: CMAP, compound muscle action potential; SRC, stimulus–response curve; TE, threshold electrotonus; CTR, current–threshold relationship; RC, recovery cycle

Received April 23, 2008. Revised June 6, 2008. Accepted July 14, 2008.


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