Basal lamina directs acetylcholinesterase accumulation at synaptic sites in regenerating muscle.

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Abstract
In skeletal muscles that were damaged in ways which spare the basal lamina sheaths of the muscle fibers, new myofibers develop within the sheaths and neuromuscular junctions form at the original synaptic sites on them. At the regenerated neuromuscular junctions, as at the original ones, the muscle fibers are characterized by junctional folds and accumulations of acetylcholine [ACH] receptors and acetylcholinesterase (AChE). The formation of junctional folds and the accumulation of Ach receptors is directed by components of the synaptic portion of the myofiber basal lamina. Whether or not the synaptic basal lamina contains molecules that direct the accumulation of AChE was determined. Frog muscles were crushed in a way that caused disintegration and phagocytosis of all cells at the neuromuscular junction, and at the same time, AChE activity was irreversibly blocked. New muscle fibers were allowed to regenerate within the basal lamina sheaths of the original muscle fibers but reinnervation of the muscles was deliberately prevented. AChE activity was stained for and the surface of the new muscle searched for deposits of enzyme they had produced. Despite the absence of innervation, AChE preferentially accumulated at points where the plasma membrane of the new muscle fibers was apposed to the regions of the basal lamina that had occupied the synaptic cleft at the neuromuscular junctions. Molecules stably attached to the synaptic portion of myofiber basal lamina direct the accumulation of AChE at the original synaptic sites in regenerating muscle. The AChE was solubilized by collagenase and that it remained adherent to basal lamina sheaths after degeneration of the new myofibers, indicating that it had become incorporated into the basal lamina, as at normal neuromuscular junctions.