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Calcium Influx and Release Cooperatively Regulate AChR Patterning and Motor Axon Outgrowth during Neuromuscular Junction Formation.
Cell Reports ( IF 7.5 ) Pub Date : 2018-06-26 , DOI: 10.1016/j.celrep.2018.05.085 Mehmet Mahsum Kaplan 1 , Nasreen Sultana 1 , Ariane Benedetti 1 , Gerald J Obermair 1 , Nina F Linde 2 , Symeon Papadopoulos 2 , Anamika Dayal 3 , Manfred Grabner 3 , Bernhard E Flucher 1
Cell Reports ( IF 7.5 ) Pub Date : 2018-06-26 , DOI: 10.1016/j.celrep.2018.05.085 Mehmet Mahsum Kaplan 1 , Nasreen Sultana 1 , Ariane Benedetti 1 , Gerald J Obermair 1 , Nina F Linde 2 , Symeon Papadopoulos 2 , Anamika Dayal 3 , Manfred Grabner 3 , Bernhard E Flucher 1
Affiliation
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Formation of synapses between motor neurons and muscles is initiated by clustering of acetylcholine receptors (AChRs) in the center of muscle fibers prior to nerve arrival. This AChR patterning is considered to be critically dependent on calcium influx through L-type channels (CaV1.1). Using a genetic approach in mice, we demonstrate here that either the L-type calcium currents (LTCCs) or sarcoplasmic reticulum (SR) calcium release is necessary and sufficient to regulate AChR clustering at the onset of neuromuscular junction (NMJ) development. The combined lack of both calcium signals results in loss of AChR patterning and excessive nerve branching. In the absence of SR calcium release, the severity of synapse formation defects inversely correlates with the magnitude of LTCCs. These findings highlight the importance of activity-dependent calcium signaling in early neuromuscular junction formation and indicate that both LTCC and SR calcium release individually support proper innervation of muscle by regulating AChR patterning and motor axon outgrowth.
中文翻译：
钙的流入和释放协同调节神经肌肉连接形成过程中的AChR模式和运动轴突的生长。
运动神经元和肌肉之间的突触形成是通过在神经到达之前在肌肉纤维中心的乙酰胆碱受体（AChRs）聚集来开始的。这种AChR模式被认为严重依赖于通过L型通道（CaV1.1）的钙流入。在小鼠中使用遗传方法，我们在这里证明L型钙流（LTCCs）或肌浆网（SR）钙释放是必要的，并且足以在神经肌肉接头（NMJ）发育开始时调节AChR簇集。两种钙信号的综合缺乏导致AChR模式丧失和神经分支过多。在没有SR钙释放的情况下，突触形成缺陷的严重程度与LTCC的大小成反比。
更新日期：2018-07-08
中文翻译：
钙的流入和释放协同调节神经肌肉连接形成过程中的AChR模式和运动轴突的生长。
运动神经元和肌肉之间的突触形成是通过在神经到达之前在肌肉纤维中心的乙酰胆碱受体（AChRs）聚集来开始的。这种AChR模式被认为严重依赖于通过L型通道（CaV1.1）的钙流入。在小鼠中使用遗传方法，我们在这里证明L型钙流（LTCCs）或肌浆网（SR）钙释放是必要的，并且足以在神经肌肉接头（NMJ）发育开始时调节AChR簇集。两种钙信号的综合缺乏导致AChR模式丧失和神经分支过多。在没有SR钙释放的情况下，突触形成缺陷的严重程度与LTCC的大小成反比。
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