Synaptotagmin I synchronizes transmitter release in mouse hippocampal neurons
Synaptotagmin I synchronizes transmitter release in mouse hippocampal neurons
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DOI：
10.1523/jneurosci.1563-04.2004
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发表时间：
2004-07-07
影响因子：
5.3
通讯作者：
Augustine, GJ
中科院分区：
文献类型：
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作者：
Nishiki, T;Augustine, GJ
我们已经问是否损失的Ca 2+传感器蛋白synaptotagmin I的突触前动作电位后释放的神经递质的总量的影响。如前所述，突触结合蛋白I基因敲除小鼠的海马神经元谷氨酸释放的快速同步成分大大减少。然而，在这些敲除的神经元中，缓慢异步组件期间释放的谷氨酸的量增加。作为这些变化的动力学释放的结果，有没有野生型和敲除神经元之间的突触前刺激后400毫秒内释放的递质总量的显着差异。荧光成像实验表明，野生型和敲除神经元采取和释放类似量的FM染料后去极化，表明正常量的突触囊泡贩运敲除神经元。这些结果表明，synaptotagmin I敲除神经元完全能够释放神经递质，释放的缓慢成分增加，以补偿快速成分的损失。因此，synaptotagmin I抑制了Ca 2+进入突触前末梢后神经递质的快速释放，并且似乎也抑制了较慢的、异步形式的递质释放。
We have asked whether loss of the Ca2+ sensor protein synaptotagmin I influences the total amount of neurotransmitter released after a presynaptic action potential. Hippocampal neurons from synaptotagmin I knock-out mice had a greatly reduced fast synchronous component of glutamate release, as reported previously. However, the amount of glutamate released during the slow asynchronous component increased in these knock-out neurons. As a result of these changes in the kinetics of release, there was no significant difference between wild-type and knock-out neurons in the total amount of transmitter released within 400 msec after a presynaptic stimulus. Fluorescence imaging experiments demonstrated that wild-type and knock-out neurons take up and release similar amounts of FM dye after depolarization, indicating normal amounts of synaptic vesicle trafficking in the knock-out neurons. These results indicate that synaptotagmin I knock-out neurons are fully capable of releasing neurotransmitter, with the increased slow component of release serving to compensate for loss of the fast component. Thus, synaptotagmin I synchronizes the rapid release of neurotransmitters after Ca2+ entry into presynaptic terminals and also appears to suppress the slower, asynchronous form of transmitter release.