Trachtenberg J T, Thompson W J
Department of Zoology, The University of Texas at Austin, Austin, Texas 78712, USA.
J Neurosci. 1997 Aug 15;17(16):6243-55. doi: 10.1523/JNEUROSCI.17-16-06243.1997.
Schwann cells (SCs) that cap neuromuscular junctions (nmjs) play roles in guiding nerve terminal growth in paralyzed and partially denervated muscles; however, the role of these cells in the day-to-day maintenance of this synapse is obscure. Neuregulins, alternatively spliced ligands for several erbB receptor tyrosine kinases, are thought to play important roles in cell-cell communication at the nmj, affecting synapse-specific gene expression in muscle fibers and the survival of terminal SCs during development. Here we show that application of a soluble neuregulin isoform, glial growth factor II (GGF2), to developing rat muscles alters terminal SCs, nerve terminals, and muscle fibers. SCs extend processes and migrate from the synapse. Nerve terminals retract from acetylcholine receptor-rich synaptic sites, and their axons grow, in association with SCs, to the ends of the muscle. These axons make effective synapses only after withdrawal of GGF2. These synaptic alterations appear to be induced by the actions of neuregulin on SCs, because SC transplants growing into contact with synaptic sites also caused withdrawal of nerve terminal branches. These results show that SCs can alter synaptic structure at the nmj and implicate these cells in the maintenance of this synapse.
包绕神经肌肉接头（nmjs）的施万细胞（SCs）在引导瘫痪和部分失神经肌肉中的神经末梢生长方面发挥作用；然而，这些细胞在该突触日常维持中的作用尚不清楚。神经调节蛋白是几种erbB受体酪氨酸激酶的可变剪接配体，被认为在神经肌肉接头处的细胞间通讯中起重要作用，影响肌纤维中突触特异性基因表达以及发育过程中终末施万细胞的存活。在此，我们表明，将可溶性神经调节蛋白异构体胶质生长因子II（GGF2）应用于发育中的大鼠肌肉会改变终末施万细胞、神经末梢和肌纤维。施万细胞伸出突起并从突触处迁移。神经末梢从富含乙酰胆碱受体的突触部位缩回，其轴突与施万细胞一起生长至肌肉末端。这些轴突仅在GGF2撤除后才形成有效的突触。这些突触改变似乎是由神经调节蛋白对施万细胞的作用诱导的，因为生长至与突触部位接触的施万细胞移植也会导致神经末梢分支缩回。这些结果表明，施万细胞可改变神经肌肉接头处的突触结构，并表明这些细胞参与该突触的维持。
