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Electrophysiologic differences between normal and dystrophic avian muscle.

S E Howlett, T B Hoekman

Experimental Neurology

|November 1, 1986

Summary

Avian muscular dystrophy shows altered muscle cell electrical activity. Dystrophic chicken muscles exhibit prolonged action potential duration, suggesting a defect in potassium channels is an early disease change.

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Area of Science:

Muscle physiology
Animal models of disease
Cellular electrophysiology

Background:

Electrophysiologic studies indicate a membrane defect in avian muscular dystrophy.
Previous research on avian dystrophy has proposed neurogenic and vascular causes.
In vitro studies show altered action potential characteristics in dystrophic avian muscle.

Purpose of the Study:

To investigate the in vivo electrophysiologic characteristics of dystrophic avian muscle.
To examine action potentials in the extensor digitorum communis muscle of normal and dystrophic chickens.
To determine if membrane or sarcolemmal defects are present in avian muscular dystrophy.

Main Methods:

Utilized a novel in vivo preparation of the extensor digitorum communis muscle.
Recorded intracellular action potentials in 8-week-old normal and dystrophic chickens.
Administered dantrolene sodium to attenuate muscle twitch for improved recording.

Main Results:

Resting membrane potential, action potential amplitude, and maximum rate of rise were similar between normal and dystrophic muscle cells.
Action potential duration at half the maximum amplitude was significantly increased in dystrophic muscle cells.
This finding of prolonged action potential duration is novel for avian muscular dystrophy.

Conclusions:

The study suggests a defect in sarcolemmal potassium conductance is an early change in avian muscular dystrophy.
The findings support a membrane defect as a key feature of avian dystrophy.
Further research into potassium channel function in avian muscular dystrophy is warranted.

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