MUSCULAR dystrophy in the mouse has long been regarded as a primary myopathy1–3, but many recent observations contradict this view. For example, reductions in the frequency of discharge4 and in the amplitude5 of miniature end-plate potentials have been reported, and McComas and Mrozek6 have shown that large numbers of muscle fibres in dystrophic tibialis anterior and gastrocnemius muscles are “functionally denervated”. These observations prompted us to make a detailed study of motor unit populations in normal and dystrophic mouse muscles.