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Calcitonin gene-related peptide regulates muscle acetylcholine receptor synthesis

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Abstract

Innervation of muscle by motoneurones induces the development of a characteristic, high density cluster of acetylcholine receptors (AChRs) at the neuromuscular junction1–4. Studies in vitro show that the accumulation of AChRs at nerve–muscle contacts results from both increased insertion of new AChRs into the muscle plasma membrane beneath nerve terminals5 and redistribution of preexisting AChRs5–7; these two modes of AChR accumulation may be separately controlled since factors have been identified that influence AChR redistribution but not synthesis8,9. Although many aspects of muscle development are regulated by nerve-dependent muscle activity10–16, junctional AChR clusters still develop when neuromuscular transmission is blocked by either curare or α-bungarotoxin1,5,6,17, suggesting that their formation is mediated by nerve-derived trophic factors other than activity. A molecule immunologically related to calcitonin gene-related peptide (CGRP-I) has been found in motoneurones in a variety of mammals including man18,19. Here we provide indirect evidence that CGRP-I may be a motoneurone-derived trophic factor that increases AChR synthesis at vertebrate neuromuscular junctions.

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New, H., Mudge, A. Calcitonin gene-related peptide regulates muscle acetylcholine receptor synthesis. Nature 323, 809–811 (1986). https://doi.org/10.1038/323809a0

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