Suppression of sprouting at the neuromuscular junction by immune sera.
Injury of afferent motor axons or pathological loss of motoneurones from the spinal cord causes the remaining axons within a muscle to sprout and to reinnervate the denervated muscle fibres. Sprouting occurs at two sites along intramuscular axons, at nodes of Ranvier (nodal sprouting) and at the neuromuscular junction (terminal sprouting). Terminal sprouting is also produced by treatment with botulinum toxin and by other agents that render muscle inactive. The muscle probably provides a signal for terminal sprouting as restoration of muscle activity by direct electrical stimulation prevents sprouting. Such a signal might be a local change on the muscle fibre surface or a 'soluble' sprouting factor, although the failure to induce terminal sprouting in one muscle by denervating adjacent muscles argues against the latter hypothesis. I now report that rabbit antisera against a 56,000 (56K)-molecular weight protein secreted by denervated rat muscle suppress botulinum toxin-induced terminal sprouting in the mouse gluteus muscle. An immune response against this protein has also been detected in serum of patients with amyotrophic lateral sclerosis (ALS), a disease in which loss of motoneurones from the spinal cord is not accompanied by the degree of sprouting and reinnervation seen in other motoneurone diseases.
D000690:Amyotrophic Lateral Sclerosis / Q000503:physiopathology*; D000818:Animals; D001905:Botulinum Toxins / Q000494:pharmacology; D006801:Humans; D008970:Molecular Weight; D009121:Muscle Denervation; D009124:Muscle Proteins / Q000276:immunology*; D009414:Nerve Growth Factors / Q000276:immunology*; D009469:Neuromuscular Junction / Q000502:physiology*; D051381:Rats
D009124:Muscle Proteins; D009414:Nerve Growth Factors; D001905:Botulinum Toxins