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首页> 外文期刊>Nature >Aberrant differentiation of neuromuscular junctions in mice lacking s-laminin/laminin beta 2.
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Aberrant differentiation of neuromuscular junctions in mice lacking s-laminin/laminin beta 2.

机译：缺少s-laminin / laminin beta 2的小鼠中神经肌肉接头的异常分化

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摘要

Synapse formation requires a complex interchange of information between the pre- and postsynaptic partners. At the skeletal neuromuscular junction, some of this information is contained in the basal lamina (BL), which runs through the synaptic cleft between the motor nerve terminal and the muscle fibre. During regeneration following injury, components of synaptic BL can trigger several features of postsynaptic differentiation in the absence of the nerve terminal, and of presynaptic differentiation in the absence of the muscle fibre. One nerve-derived component of synaptic BL, agrin, is known to affect postsynaptic differentiation, but no muscle-derived components have yet been shown to influence motor nerve terminals. A candidate for such a role is s-laminin (also called laminin beta 2), a homologue of the B1 (beta 1) chain of the widely distributed BL glycoprotein, laminin. s-Laminin is synthesized by muscle cells and concentrated in synaptic BL. In vitro, recombinant s-laminin fragments are selectively adhesive for motor neuron-like cells, inhibit neurite outgrowth promoted by other matrix molecules, and act as a 'stop signal' for growing neurites. By generating and characterizing mice with a targeted mutation of the s-laminin gene, we show here that s-laminin regulates formation of motor nerve terminals.
机译：突触形成需要突触前和突触后伙伴之间复杂的信息交换。在骨骼神经肌肉接头处，某些信息包含在基底层（BL）中，基底层穿过运动神经末梢与肌肉纤维之间的突触间隙。在损伤后的再生过程中，突触BL的成分可在神经末梢缺失时触发突触后分化的某些特征，而在缺乏肌肉纤维时触发突触前分化的一些特征。已知突触BL的一种神经源成分，即凝集素会影响突触后分化，但尚未显示出肌肉源成分会影响运动神经末梢。 s-laminin（也称为层粘连蛋白β2）是这种作用的候选者，它是广泛分布的BL糖蛋白层粘连蛋白的B1（β1）链的同源物。 s-层粘连蛋白由肌肉细胞合成并在突触BL中浓缩。在体外，重组s-laminin片段可选择性粘附于运动神经元样细胞，抑制其他基质分子促进的神经突向外生长，并充当神经突生长的“终止信号”。通过生成和表征具有s-laminin基因的定向突变的小鼠，我们在这里显示s-laminin调节运动神经末梢的形成。

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