Molecules in basal lamina that direct the formation of synaptic specializations at neuromuscular junctions.
Molecules in basal lamina that direct the formation of synaptic specializations at neuromuscular junctions.
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基底层中指导神经肌肉接头处突触特化形成的分子。
DOI：
10.1159/000111903
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发表时间：
1989
影响因子：
2.9
通讯作者：
Wallace,BG
中科院分区：
文献类型：
--
作者：
McMahan,UJ;Wallace,BG
在胚胎发育过程中，发育中的运动轴突终末和肌纤维交换的信号导致形成一种高度专门化的结构，用于有效的突触传递使命，即神经肌肉接头。一个重要的线索，身份的分子，可能作为一个这样的信号已经来自实验再生肌肉的成人。在成人神经肌肉接头的突触间隙中，发现基底层含有引起细胞表面特化的分子，这些分子在再生轴突终末和肌纤维中引起细胞表面特化，这些轴突终末和肌纤维类似于发育过程中形成的轴突终末和肌纤维。例如，突触基底层诱导再生轴突终末形成活性区，其参与递质乙酰胆碱的释放，并且其指导再生肌纤维形成乙酰胆碱受体（AChR）和乙酰胆碱酯酶（AChE）的聚集体。在过去的几年里，我们进行了旨在鉴定和表征诱导AChR和AChE聚集的基底层分子的实验。我们的结果导致了以下假设：（1）单个基底层分子引起AChR和AChE以及突触后器的其他成分的聚集;（2）活性分子由运动神经元合成并由其轴突终末释放以掺入基底层，以及（3）指导再生肌纤维上突触后装置形成的基底层分子与介导神经-在胚胎中，它可以诱导发育中的肌纤维形成突触后特化，并有助于维持正常成年人成熟肌纤维的特化。我们的研究进一步表明，活性分子是相同的，或非常相似，聚集蛋白，我们已经从电鳐的电器官纯化的蛋白质。在这里，我们讨论支持这些假设的证据，
During embryogenesis signals exchanged by developing motor axon terminals and myofibers lead to the formation of a structure highly specialized for effective synaptic trans mission, the neuromuscular junction. An im portant clue to the identity of a molecule that may act as one such signal has come from ex periments on regenerating muscles in the adult. The basal lamina in the synaptic cleft of adult neuromuscular junctions has been found to contain molecules that cause the for mation of cell surface specializations in re generating axon terminals and muscle fibers which resemble those formed during devel opment. For example, the synaptic basal lamina induces regenerating axon terminals to form active zones, which are involved in the release of the transmitter, acetylcholine, and it directs regenerating muscle fibers to form aggregates of acetylcholine receptors (AChRs) and acetylcholinesterase (AChE). Over the last several years we have con ducted experiments aimed at identifying and characterizing the basal lamina molecules that induce the aggregation of AChRs and AChE. Our results have led to the follow ing hypotheses:(1) A single basal lamina molecule causes the aggregation of both AChRs and AChE as well as other compo nents of the postsynaptic apparatus;(2) the active molecule is synthesized by motor neurons and released by their axon terminals to be incorporated into the basal lamina, and (3) the basal lamina molecule that directs for mation of the postsynaptic apparatus on re generating muscle fibers is the same molecule that mediates the nerve-induced formation of postsynaptic specializations on developing muscle fibers in the embryo and it helps maintain those specializations on mature muscle fibers in the normal adult. Our studies indicate further that the active molecule is identical, or very similar, to agrin, a protein we have purified from the electric organ of Torpedo californica. Here we discuss evi dence that supports these hypotheses and