Compound muscle action potential (CMAP) is an electrophysiological technique commonly employed to monitor the functional status of muscles in anesthetized animals. CMAP measurements offer insight into physiological development as well as degeneration of the peripheral neuromuscular system. As part of the electromyographic (EMG) evaluation, CMAP is regularly used in diagnostic and clinical human studies, providing a clear translational value. The recording procedure consists of stimulating a motor nerve with a supramaximal stimulus and recording the response from the muscle.
Changes in various CMAP characteristics can reflect the loss of motor axons, decreased speed of signal transmission along the nerve or muscle weakening and are therefore directly relevant to neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS), Parkinson’s disease, and even Alzheimer’s disease and lysosomal storage diseases such as Pompe disease.
CMAP evaluation of the SOD1-G93A ALS mouse model results in a severely reduced maximal CMAP response (Figure 1 A), an increased latency to onset (Figure 1 B) and regular CMAP duration (Figure 1 C), pointing towards degeneration of motor axons and a decreased speed of signal transmission from the nerve to the muscle, with a physiological synchrony between muscle fibers. The muscles of SOD1-G93A mice also exhibited a decrease in the CMAP amplitude after repeated stimulation (Figure 2), indicating muscle weakening due to pathological changes of the neuromuscular junction.
Figure 1: Compound Muscle Action Potential (CMAP) in gastrocnemius muscle of SOD1-G93A mice. Maximal CMAP amplitude (A), latency to CMAP onset (B), CMAP duration (C) and the ratio between CMAP duration and amplitude (D). Unpaired t-test. n= 8 per group. Mean + SEM. **p<0.01.
Figure 2: Weakening of the gastrocnemius muscle in SOD1-G93A mice. Change in elicited response when comparing the 1st response with the 5th (A) and the 10th response (B). Unpaired t-test. n= 6 per group. Mean + SEM. *p<0.05.
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