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The electrical “cable” properties of fibers in the soleus muscle of normal and dystrophic mice were measured in vitro at 37C with intracellular microelectrodes. The motor nerve of the dystrophic muscle was stimulated to determine whether or not the fibers chosen for measurement were functionally innervated. Normal and dystrophic muscles which had been surgically denervated were also studied. Specific membrane resistance was higher in normal than in dystrophic muscle fibers; the respective mean values were 1516 and 636 ohm cm 2 . Dystrophic fibers which were not functionally innervated had significantly higher resistance than those which were innervated, but in neither case did values approach the normal. In both normal and dystrophic muscles, previous sectioning of the motor nerve led to an increase in muscle fiber input resistance. Surgically denervated dystrophic fibers had considerably higher resistance than measured in fibers which had become functionally denervated during the course of the disease. The results suggest that denervation per se cannot account for the differences between normal and dystrophic muscle fibers.

The ability of dystrophic soleus muscle fibers to generate action potentials in response to supramaximal nerve stimulation was studied with intracellular microelectrodes in mice of the Bar Harbor 129- ReJ dy strain. In experiments conducted in vivo at either 23 or 37 C, about 55% of the fibers examined were abnormal in their ability to generate action potentials. Some of these fibers showed no detectable response to stimulation of the motor nerve, whereas in others, abortive spikes or localized end-plate potentials were recorded. The proportion of fibers showing very small or no electrical response increased when recordings were made away from the end-plate zone. Reinnervated normal muscle fibers examined 1.5 months after microcauterization of the end-plate region often responded to nerve stimulation with abortive spikes. “Functional denervation” is discussed in terms of presynaptic and postsynaptic defects.

This paper is concerned with both the quantitative information and the theory required for the interpretation of certain experimental results obtained with intracellular microelectrodes. The theory treats the spread of current from a neuron soma into branching dendritic trees. Formulas are derived for the calculation of membrane resistivity from physiological measurements of whole neuron resistance and anatomical measurements of soma and dendritic dimensions. The variability of available anatomical and physiological information is discussed. The numerical result is an estimated range of membrane resistivity values for mammalian motoneurons, and a corresponding set of values for the dendritic to soma conductance ratio. These values are significantly greater than those currently accepted in the literature, mainly because the dendritic dimensions appear to have been underestimated previously. Analysis of the histological evidence also reveals significant quantitative differences between infant, adult, and chromatolytic motoneurons. The theory builds upon the classical theory of axonal membrane electrotonus; all important assumptions are explicitly stated and discussed. The theory is general and can be applied to many types of neurons with many types of dendritic trees; it is also relevant to the diffusion of material in neurons. The 3 2 power of dendritic trunk diameter is shown to be a fundamental index of dendritic size. Another parameter characterizes the extensiveness of dendritic branching.