Ca(2+)-dependent enhancement of release by subthreshold somatic depolarization.
Ca(2+)-dependent enhancement of release by subthreshold somatic depolarization.
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DOI：
10.1038/nn.2718
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发表时间：
2011-01
影响因子：
25
通讯作者：
Jahr, Craig E.
中科院分区：
文献类型：
--
作者：
Christie, Jason M.;Chiu, Delia N.;Jahr, Craig E.
在许多神经元中，阈下躯体去极化可以电紧张性地传播到轴突中并调节随后的棘波诱发的传递。虽然释放概率是由细胞内钙离子调节，这种调节机制的钙依赖性一直存在争议。使用成对的记录从突触连接的分子层中间神经元（MLI）的大鼠小脑，我们观察到钙离子介导的加强释放短暂的阈下去极化的索马。双光子显微镜显示，在轴突，体细胞去极化诱发钙离子内流通过电压敏感性钙通道（VSCC）和促进尖峰诱发的钙离子进入。外源性Ca2+缓冲减少这些Ca2+瞬变和消除加强释放。亚阈值躯体去极化引起的轴突Ca2+进入也引发了异步传输，可能会耗尽囊泡的可用性，从而加强脾气释放。在这个小脑回路中，活动依赖性突触前可塑性依赖于由索马启动的阈下和阈上电活动引起的Ca 2+升高。
In many neurons, subthreshold somatic depolarization can spread electrotonically into the axon and modulate subsequent spike-evoked transmission. Although release probability is regulated by intracellular Ca2+, the Ca2+-dependence of this modulatory mechanism has been debated. Using paired recordings from synaptically connected molecular-layer interneurons (MLIs) of the rat cerebellum, we observed Ca2+-mediated strengthening of release following brief subthreshold depolarization of the soma. Two-photon microscopy revealed that, at the axon, somatic depolarization evoked Ca2+ influx through voltage-sensitive Ca2+ channels (VSCCs) and facilitated spike-evoked Ca2+ entry. Exogenous Ca2+ buffering diminished these Ca2+ transients and eliminated the strengthening of release. Axonal Ca2+ entry elicited by subthreshold somatic depolarization also triggered asynchronous transmission that may deplete vesicle availability and thereby temper release strengthening. In this cerebellar circuit, activity-dependent presynaptic plasticity depends on Ca2+ elevations resulting from both sub- and suprathreshold electrical activity initiated at the soma.
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