Influence of innervation on molecular forms of acetylcholinesterase in regenerating fast and slow skeletal muscles

Nerve-intact muscle regenerates were prepared by ischemic-toxic injury of slow soleus (SOL) and fast extensor digitorum longus (EDL) muscles of the rat. Rapid innervation of regenerating myotubes modified intrinsic patterns of AChE molecular forms, revealed by velocity sedimentation in linear sucrose gradients. Regarding their onset, the effects of innervation can be classified as early and late. The earliest changes in the SOL regenerates appeared a few clays after inner vation by their motoneurons: The activity of the 13 S AChE form (A 8) increased significantly in compari son to non-innervated regenerates. The pattern of AChE molecular forms became similar to that in the normal SOL muscle during the 2nd week after in jury. In contrast, no major differences were observed between 8 day-old innervated and non-innervated EDL regenerates. Their patterns of AChE molecular forms resembled that in the normal EDL. However, the predominance of the 10 S AChE form (G 4) char acteristic for the 2-week old non-innervated regener ates was prevented by innervation. Early effect of innervation observed in the SOL regenerates but not in the EDL may be due to intrinsically different re sponse of the regenerating SOL myotubes to innerva tion. Rather high extrajunctional activity of the asymmetric 16 S (A 12) molecular form of AChE in early regenerates was reduced to adult level in about 3 weeks in the SOL, and nearly completely sup pressed in 5 weeks after innervation in the EDL re generates. This reduction is assumed to be a late ef fect of innervation, as well as a decrease of the activity of the 4 S AChE form (G 1) in the SOL regenerates. A suppressive mechanism is activated in the extra junctional regions of the innervated muscle regener ates during their maturation. This mechanism coun teracts the enhancing influence of contractile activity on the expression of the asymmetric AChE forms in immature muscle cells, and is more efficient in the EDL than in the SOL. Its onset may be apparently delayed by protracted fusion of the satellite cells with muscle fibers.