Abstract

Focal accumulations of E-face intramembranous particles occur in spinal cord axons of myelin-deficient rat mutants. These resemble nodal particles and, like them, may represent voltage-sensitive sodium channels. It is proposed that axonal activity at these foci could increase extracellular potassium to the point of triggering activity in adjacent axons. Rapid spread of such potassium-induced activity among bare axons could underlie the seizures and other neurological abnormalities that develop in this mutant. A similar mechanism may account for the paroxysmal attacks sometimes seen in multiple sclerosis.

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