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A synaptic laminin–calcium channel interaction organizes active zones in motor nerve terminals

Author

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  • Hiroshi Nishimune

    (Washington University School of Medicine
    Harvard University)

  • Joshua R. Sanes

    (Washington University School of Medicine
    Harvard University)

  • Steven S. Carlson

    (University of Washington)

Abstract

Synapse formation requires the differentiation of a functional nerve terminal opposite a specialized postsynaptic membrane. Here, we show that laminin β2, a component of the synaptic cleft at the neuromuscular junction, binds directly to calcium channels that are required for neurotransmitter release from motor nerve terminals. This interaction leads to clustering of channels, which in turn recruit other presynaptic components. Perturbation of this interaction in vivo results in disassembly of neurotransmitter release sites, resembling defects previously observed in an autoimmune neuromuscular disorder, Lambert–Eaton myasthenic syndrome. These results identify an extracellular ligand of the voltage-gated calcium channel as well as a new laminin receptor. They also suggest a model for the development of nerve terminals, and provide clues to the pathogenesis of a synaptic disease.

Suggested Citation

  • Hiroshi Nishimune & Joshua R. Sanes & Steven S. Carlson, 2004. "A synaptic laminin–calcium channel interaction organizes active zones in motor nerve terminals," Nature, Nature, vol. 432(7017), pages 580-587, December.
    • Handle: RePEc:nat:nature:v:432:y:2004:i:7017:d:10.1038_nature03112
    DOI: 10.1038/nature03112
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