Schwann Cells

The role of Schwann cells in NMJ stability should not be overlooked. The Schwann cells migrate along the motor axons and arrive at the synapse immediately after the axons themselves contact the muscle. If Schwann cells fail to migrate, the early connections formed by the motor axons quickly degenerate, and the axons retract74,75. This presumably reflects a critical trophic role for Schwann cells in maintaining the viability of the axon. In adulthood, Schwann cells are also essential for NMJ plasticity. Sprouts from the terminal Schwann cell of a denervated NMJ seek neighboring active synapses and stimulate the neighboring motor neurons to sprout and reinnervate the lost junction76,77. Thus, Schwann cells are essential for the process as a whole, but the intimate interactions between motor axons and the glia make it difficult to determine whether the effects are directly attributable to the Schwann cell, or whether the Schwann cell is indirectly enabling the motor axon to form and maintain its connections. A role for glia in synapse formation, stabilization, and plasticity is undoubtedly a shared feature of NMJs and CNS synapses78.

Numerous other systems are just beginning to be explored. Integrins are present at the NMJ and may well play a role in its development79, but their analysis is complicated by their function in many developmental pathways, which often obscure their effect on synaptogenesis. Similarly, synapse-specific glycosylation is also intriguing as a possible mechanism through which synapses may be organized or stabilized80. Studies of this are underway, but are technically challenging. The importance of glycosyltransferases for the neuromuscular system is established by diseases such as Fukuyama's muscular dystrophy, muscle-eye-brain disease, and the Large mutations in mice81-83. While some aspects of these diseases may be attributed to improper glycosylation of dystroglycan, a comprehensive understanding of the substrates and mechanisms of these enzymes remains to be achieved.

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