ABSENCE OF DYSTROPHIC CHARACTERISTICS IN NORMAL MUSCLES SUCCESSFULLY CROSS-REINNERVATED BY NERVES OF DYSTROPHIC GENOTYPE - PHYSIOLOGICAL AND CYTOCHEMICAL STUDY OF CROSSED SOLEI OF NORMAL AND DYSTROPHIC PARABIOTIC MICE

Dystrophic mice and normal littermates were joined in parabiotic union between 20-23 days of age with a cross of the last tibial nerve of 1 partner to the slow soleus muscle of the other. This preparation allowed monitoring of the neurotrophic influences of fast nerves on slow muscles and assessment of the influence of these nerves on the expression of hereditary muscular dystrophy. Twelve parabiotic pairs examined 3-6 mo. postoperatively reveal that the cross-reinnervated solei, either normal or dystrophic, exhibit post-tetanic potentiation, a mean 30% decrease in contraction time, and a mean 48% decrease in half-relaxation time as compared to the contralateral control, self-reinnervated muscles. Self-reinnervated dystrophic solei generate 60% less tension than do self-reinnervated normal solei. The contractile capabilities of solei of the dystrophic mice cross-reinnervated by nerves of the normal partners are not enhanced and these parameters were not reduced in normal solei receiving nerves of dystrophic genotype. Cross-reinnervated solei exhibited twitch and tetanic tension similar to those of their contralateral control muscles. Cytochemical and structural analyses indicated that the crossed fast nerves of normal or of dystrophic genotype are effective in altering the cytochemical pattern of the slow muscles to fiber types characteristic of fast muscles. Normal nerves innervating solei of the dystrophic parabiont do not arrest the progress of the disease, and nerves of dystrophic genotype innervating muscles of the normal parabiont do not induce a pathological state. The peripheral motor nerves of dystrophic mice are normal in exerting neurotrophic influences; muscular dystrophy progresses in spite of the presence of normal neurotrophic influences. This double nerve parabiotic cross suggests that the etiology of hereditary muscular dystrophy in this species is not nerve mediated.