Delayed Synaptic Transmission in Drosophila cacophonynull Embryos
Delayed Synaptic Transmission in Drosophila cacophonynull Embryos
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DOI：
10.1152/jn.90342.2008
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发表时间：
2008-11-01
影响因子：
2.5
通讯作者：
Kidokoro, Yoshiaki
中科院分区：
文献类型：
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作者：
Hou, Jiamei;Tamura, Takuya;Kidokoro, Yoshiaki
张文忠，张文忠.果蝇杂音（无效）胚胎中的延迟交感传递。神经生理学杂志100：2833-2842，2008年。首次发表于2008年9月24日; doi：10.1152/jn.90342.2008。钙离子通过果蝇的N型钙通道内流，由杂音（cac）编码，触发快速突触传递。我们现在要问的是，cac Ca 2+通道是否是专门用于快速突触传递的Ca 2+通道。因为cac（无效）突变是致命的，我们使用cac（无效）胚胎来解决这个问题。在HL 3溶液中的神经肌肉接头处，神经刺激时未检测到快速同步突触传递。当野生型cac基因被引入cac（null）背景中时，快速突触传递恢复。然而，即使在cac（null）胚胎中，神经刺激也很少在1.5 mM [Ca 2 +]（e）的少数细胞和5 mM [Ca 2 +]（e）的大多数细胞中诱导延迟的突触事件。在5 mM [Ca ~（2+）]（e）浓度下，每刺激延迟量子事件的数目大于在1.5mM [Ca ~（2+）]（e）浓度下，因此延迟释放是[Ca ~（2+）]（e）依赖性的。Plectreurys毒素II（PLTXII）（10 nM;蜘蛛毒素类似物）抑制延迟事件的频率，表明电压门控Ca 2+通道，而不是cac Ca 2+通道，对它们有贡献。然而，延迟事件不受50 μ M La 3+的影响。在cac（null）胚胎中，微突触电流频率为对照的1/2，而在高K+溶液中，微突触电流频率为对照的1/135。高渗反应与对照组的1/10相似。这些发现表明，在cac（null）胚胎中，准备释放的囊泡数量较少。总之，cac Ca 2+通道在正常条件下对于快速突触传递是必不可少的，并且另一种类型的Ca 2+通道，非cac的PLTXII敏感的Ca 2+通道，有助于cac（null）胚胎中的延迟释放。
Hou J, Tamura T, Kidokoro Y. Delayed symaptic transmission in Drosophila cacophony(null) embryos. J Neurophysiol 100: 2833-2842, 2008. First published September 24, 2008; doi: 10.1152/jn.90342.2008. Ca2+ influx through the Drosophila N-type Ca2+ channel, encoded by cacophony (cac), triggers fast synaptic transmission. We now ask whether the cac Ca2+ channel is the Ca2+ channel solely dedicated for fast synaptic transmission. Because the cac(null) mutation is lethal, we used cac(null) embryos to address this question. At the neuromuscular junction in HL3 solution, no fast synchronous synaptic transmission was detected on nerve stimulation. When the wild-type cac gene was introduced in the cac(null) background, fast synaptic transmission recovered. However, even in cac(null) embryos, nerve stimulation infrequently induced delayed synaptic events in the minority of cells in 1.5 mM [Ca2+](e) and in the majority of cells in 5 mM [Ca2+](e). The number of delayed quantal events per stimulus was greater in 5 mM [Ca2+](e) than in 1.5 mM. Thus the delayed release is [Ca2+](e) dependent. Plectreurys toxin II ( PLTXII) ( 10 nM; a spider toxin analog) depressed the frequency of delayed events, suggesting that voltage-gated Ca2+ channels, other than cac Ca2+ channels, are contributing to them. However, delayed events were not affected by 50 mu M La3+. The frequency of miniature synaptic currents in cac(null) embryos was similar to 1/2 of control, whereas in high K+ solutions, it was similar to 1/135. The hypertonicity response was similar to 1/10 of control. These findings indicate that the number of release-ready vesicles is smaller in cac(null) embryos. Taken together, the cac Ca2+ channel is indispensable for fast synaptic transmission in normal conditions, and another type of Ca2+ channel, the non-cac, PLTXII-sensitive Ca2+ channel, is contributing to delayed release in cac(null) embryos.