[Formation and repression of neuromuscular endplates in neurogenic and muscular lesions]

The motor endplates and intramuscular nerves of rat and rabbit masticatory muscle were preferentially demonstrated using an acetylcholinesterase reaction followed by silver staining. The regeneration of the neuromuscular unit was followed serially at the site of an earlier biopsy. Using observations concerning the sproutings of neuronal fibers in normal and operated animals, a hypothetical generalization of the phenomenon is proposed and evaluated in the light of the literature. Intramuscular sprouts of motor axons are detectable both in normal and partially denervated muscle. These can be regarded as the precondition of the muscle's ability to adapt to an altered stress situation. Single muscle fibers and synapses are multiply innervated by different alpha-motor neurons with subsequent fiber transformation via an intermediary stage, the 2C fiber. Following neurogenic damage a trigger is released from the denervated muscle tissue and damaged nerve parenchyma which stimulates the reinnervation of surviving motor endplates by axon sprouting and new synapse formation. Collateral, nerve stem, and terminal sprouts may occur singly or multiply. As long as denervated muscle fibers are present triggers for synapse formation and axon sprouting, as opposed to repression, continue to be released, resulting in a period of poly-innervation. The degree of sprouting correlates with the extent of nerve damage. The period of innervation is not affected by muscle damage alone. Complete or partial fiber regeneration products will survive only if they reach an innervation zone where neurotransmission is insured by the presence of sprouts and synapses. The period of poly-innervation is followed by a period of synapse repression whereby the redundant sprouts and synapses are reabsorbed. The length of the axon determines the sprouts resistance to reabsorption. The connections which survive are those which are the shortest between the endplate and the stem nerve. Intramuscular sprouting can be experimentally stimulated by, among other factors, partial denervation, oxygen deficiency, toxic inactivation, an altered stress situation and exogenous gangliosides.