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Abstract
The neuromuscular junction (NMJ) is a well-studied chemical synapse and has served as a tractable model system to clarify how synapse formation occurs. Proteins on both the presynaptic and postsynaptic sides collaborate to induce the high-density accumulation of acetylcholine receptors (AChRs) at the NMJ. Two opposing pathways work in this process: A dispersing pathway works through acetylcholine and the AChR, and a clustering pathway works through agrin and the transmembrane tyrosine kinase MuSK. The molecular mechanisms underlying these two signaling cascades are beginning to be understood.
