Calcitonin gene-related peptide regulates muscle acetylcholine receptor synthesis
Innervation of muscle by motoneurones induces the development of a characteristic, high density cluster of acetylcholine receptors (AChRs) at the neuromuscular junction 1–4 . Studies in vitro show that the accumulation of AChRs at nerve–muscle contacts results from both increased insertion of new AC...
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Veröffentlicht in: | Nature (London) 1986-10, Vol.323 (6091), p.809-811 |
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Sprache: | eng |
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Zusammenfassung: | Innervation of muscle by motoneurones induces the development of a characteristic, high density cluster of acetylcholine receptors (AChRs) at the neuromuscular junction
1–4
. 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 terminals
5
and redistribution of preexisting AChRs
5–7
; these two modes of AChR accumulation may be separately controlled since factors have been identified that influence AChR redistribution but not synthesis
8,9
. Although many aspects of muscle development are regulated by nerve-dependent muscle activity
10–16
, junctional AChR clusters still develop when neuromuscular transmission is blocked by either curare or
α
-bungarotoxin
1,5,6,17
, 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 man
18,19
. 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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ISSN: | 0028-0836 1476-4687 |
DOI: | 10.1038/323809a0 |