Section 7
Chapter 6,156

Potassium channel distribution in spinal root axons of dystrophic mice

Bostock, H.; Rasminsky, M.

Journal of Physiology 340: 145-156


ISSN/ISBN: 0022-3751
PMID: 6310095
DOI: 10.1113/jphysiol.1983.sp014755
Accession: 006155991

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We have used 4-aminopyridine (4AP), a potassium channel blocker, to assess the presence and distribution of potassium channels in the congenitally abnormally myelinated spinal root axons of dystrophic mice. 1 mM-4AP slightly depressed the amplitude but had no effect on the half-width of the monophasic action potential of normal A fibres, indicating the absence of a significant concentration of potassium channels at normal mouse nodes of Ranvier. By progressively increasing stimulus intensity it was possible to elicit three more or less discrete components of the compound action potential from dystrophic mouse spinal roots, presumably corresponding to myelinated fibres, large diameter bare axons and, in the case of dorsal roots, C fibres. The amplitude and duration of all three components were increased on exposure to 4AP, indicating the presence of potassium channels in all types of dystrophic mouse spinal root axons. Conduction in single fibres was studied using longitudinal current analysis. Both saltatory and continuous conduction were observed corresponding to the myelinated and bare portions of dystrophic mouse spinal root axons. Three types of 'nodal' membrane could be inferred from the membrane current recordings from myelinated dystrophic mouse axons: (1) pure sodium channel membrane, (2) membrane containing both sodium and potassium channels, and (3) membrane containing predominantly, if not exclusively, potassium channels. The large early outward currents at the latter two types of nodes suggested that these nodes were wider than normal. Recordings of continuous conduction indicated that potassium channels were also distributed irregularly along bare portions of the dystrophic mouse axons. These abnormalities of ion channel distribution are interpreted as reflecting failure of normal axon-Schwann cell communication in the dystrophic mouse spinal roots.

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