作者: Helen V. New , Anne W. Mudge
DOI: 10.1038/323809A0
关键词: Acetylcholine receptor 、 Cell biology 、 Curare 、 Calcitonin 、 Calcitonin gene-related peptide 、 Muscarinic acetylcholine receptor M5 、 Chemistry 、 Muscarinic acetylcholine receptor M3 、 Neuromuscular transmission 、 Calcitonin receptor
摘要: Innervation of muscle by motoneurones induces the development a characteristic, high density cluster acetylcholine receptors (AChRs) at neuromuscular junction1–4. Studies in vitro show that accumulation AChRs nerve–muscle contacts results from both increased insertion new into plasma membrane beneath nerve terminals5 and redistribution preexisting AChRs5–7; these two modes AChR may be separately controlled since factors have been identified influence but not synthesis8,9. Although many aspects are regulated nerve-dependent activity10–16, junctional clusters still develop when transmission is blocked either curare or α-bungarotoxin1,5,6,17, suggesting their formation mediated nerve-derived trophic other than activity. A molecule immunologically related to calcitonin gene-related peptide (CGRP-I) has found variety mammals including man18,19. Here we provide indirect evidence CGRP-I motoneurone-derived factor increases synthesis vertebrate junctions.