MUSCLE TRANSPLANTATION BETWEEN NORMAL AND DYSTROPHIC MICE. 2. HISTOCHEMICAL STUDIES

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Abstract
Innervated and denervated auto‐ and crosstransplants, ranging in age from 1 hour to over 300 days, of normal and dystrophic tibialis anterior muscles in 129 ReJ mice have been examined histochemically for oxidative and glycolytic enzymes, ATPase, acetylcholinesterase, glycogen and nucleic acids. All transplants were devoid of glycogen and phosphorylase activity within 12 hours of transplantation. Fibre types were distinguished in the central areas of 2 day old transplants with NADH‐TR and ATPase reactions, but at the periphery, where fibres were at a rnore advanced stage of degeneration, fibre typing was not evident and NADH‐TR and ATPase reaction products were clumped. By 3 to 4 days most implanted fibres had broken down, but NADH‐TR and ATPase activity were still evident. “yotubes were observed in areas of 3 day old transplants where muscle fibres had completely degenerated and these stained uniformly for RNA, NADH‐TR and ATPase. Phosphorylase activity and glycogen were first observed in myotubes of 8 day old transplants. When examined before 12 days, myotubes of all transplants showed uniform NADH‐TR, ATPase, phosphorylase and RNA. Subsequently NADH‐TR, ATPase and PAS reactions showed progressive differentiation of type 1 and 2 fibres in innervated normal and dystrophic transplants in normal mice. All transplants in normal and in dystrophic mice, denervated at the time of transplantation, failed to show fibre type differentiation. Despite substantial regeneration before 25 days, all transplants in dystrophic mice subsequently underwent progressive degeneration. A similar pattern was observed in denervated transplants in normal mice. The few fibres that remained in these transplants showed uniform NADH‐TR and ATPase activity, whilst phosphorylase and glycogen were absent. Innervated normal and dystrophic transplants in normal mice showed maintenance of differentiated type 1 and 2 fibres even after 300 days, thus resembling intact normal rather than intact dystrophic muscles. This study supports the view that murine muscular dystrophy may have a neural basis for its pathogenesis.