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Brain, Vol. 118, No. 5, 1225-1231, 1995
© 1995 Guarantors of Brain

research-article

A mechanism for ectopic firing in central demyelinated axons

Paul A. Felts1, Raju Kapoor2 and Kenneth J. Smith1

1 Department of Neurology and Division of Anatomy and Cell Biology, United Medical and Dental Schools of Guy's and St Thomas' Hospitals, Guy's Campus London, UK 2 University Department of Clinical Neurology, The Institute of Neurology London, UK

Correspondence to: Dr K. J. Smith, Department of Neurology, UMDS-Guy's Campus, London SE1 9RT, UK

Intracellular recordings of ectopic activity were made from demyelinated axons in rat dorsal columns using in vitro techniques. On-going bursts of discharges were observed in some axons, and these were sometimes superimposed upon slow depolarizing potentials. These intracellularly recorded, depolarizing potentials were strongly reminiscent of the slow negative potentials previously recorded extracellularly from the periaxonal region of normal myelinated fibres following potassium loading of this space. Also, in previously silent demyelinated axons, ectopic activity could sometimes be induced by brief periods of high frequency stimulation applied remotely from the lesion. The generation of the ectopic activity can be explained in terms of an artificially increased periaxonal concentration of potassium which may lead to the opening of internodal potassium channels and an inward potassium current. We suggest that a raised periaxonal potassium concentration may occur within compartments in demyelinating lesions, and that it can result in the generation of ectopic impulses.

action potentials; potassium channels; multiple sclerosis; central nervous system; positive symptoms

Received January 4, 1995. Revised May 1, 1995. Accepted May 28, 1995.


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