Synaptic transmission and plasticity are modulated by nonmuscle myosin II at the neuromuscular junction of Drosophila
Synaptic transmission and plasticity are modulated by nonmuscle myosin II at the neuromuscular junction of Drosophila
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DOI：
10.1152/jn.00718.2010
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发表时间：
2011-05-01
影响因子：
2.5
通讯作者：
Stewart, Bryan A.
中科院分区：
文献类型：
--
作者：
Seabrooke, Sara;Stewart, Bryan A.
西布鲁克·S，斯图尔特学士。果蝇神经肌肉连接处的突触传递和可塑性受非肌肉肌球蛋白II的调节。神经生理学杂志105：1966-1976,2011年。2011年2月16日首次出版；DOI：10.1152/jn.00718.2010。-神经末梢中的突触小泡群体传统上根据生理标准分为亚群体；容易释放池(Rrp)、回收池和备用池。人们认识到，RRP从属于低频神经活动引起的突触传递，随着神经活动的增加，循环和储备群体被要求提供囊泡。在这里，我们研究了非肌肉肌球蛋白II(NMMII)在突触传递中的作用，重点是运动蛋白在囊泡供应中的作用。我们使用果蝇遗传学来操纵NMMII，并评估了幼虫神经肌肉连接处的突触传递。我们观察到低频刺激下突触强度与NMMII表达呈正相关：减少NMMII会降低诱发反应，而增加NMMII会增加诱发反应。此外，我们发现NMMII对囊泡自发释放的贡献不同于诱发释放，这表明NMMII对这两种释放机制的贡献不同。通过测定生理盐水中不同外界钙浓度条件下的突触反应，我们发现NMMII对于高频刺激下正常的突触传递是重要的。这项研究确定了NMMII在突触传递中的不同功能，并表明这种运动蛋白在突触小泡招募的生理学中起着积极的作用。
Seabrooke S, Stewart BA. Synaptic transmission and plasticity are modulated by nonmuscle myosin II at the neuromuscular junction of Drosophila. J Neurophysiol 105: 1966-1976, 2011. First published February 16, 2011; doi:10.1152/jn.00718.2010.-The synaptic vesicle population in a nerve terminal is traditionally divided into sub-populations according to physiological criteria; the readily releasable pool (RRP), the recycling pool, and the reserve pool. It is recognized that the RRP subserves synaptic transmission evoked by low-frequency neural activity and that the recycling and reserve populations are called on to supply vesicles as neural activity increases. Here we investigated the contribution of nonmuscle myosin II (NMMII) to synaptic transmission with emphasis on the role a motor protein could play in the supply of vesicles. We used Drosophila genetics to manipulate NMMII and assessed synaptic transmission at the larval neuromuscular junction. We observed a positive correlation between synaptic strength at low-frequency stimulation and NMMII expression: reducing NMMII reduced the evoked response, while increasing NMMII increased the evoked response. Further, we found that NMMII contributed to the spontaneous release of vesicles differentially from evoked release, suggesting differential contribution to these two release mechanisms. By measuring synaptic responses under conditions of differing external calcium concentration in saline, we found that NMMII is important for normal synaptic transmission under high-frequency stimulation. This research identifies diverse functions for NMMII in synaptic transmission and suggests that this motor protein is an active contributor to the physiology of synaptic vesicle recruitment.