Facilitation of presynaptic calcium currents in the rat brainstem
Facilitation of presynaptic calcium currents in the rat brainstem
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DOI：
10.1111/j.1469-7793.1998.149by.x
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发表时间：
1998-11-15
影响因子：
5.5
通讯作者：
Sakmann, B
中科院分区：
文献类型：
--
作者：
Borst, JGG;Sakmann, B
1.为了研究突触前Ca2+内流的使用依赖性变化及其对递质释放的贡献，我们在大鼠听性脑干脑片上同时记录了突触前终末（Held的萼）和突触后细胞（斜方体内侧核的主要细胞）的电压钳记录.在短（2 ms）预脉冲至0 mV后，钙通道在负测试电位的步骤中打开得更快。在动作电位波形的序列中，每个动作电位的Ca 2+内流增加。与此同时，EPSC的振幅也降低.钙电流的促进似乎取决于细胞内Ca2+的积累，因为其幅度与Ca2+内流成比例，并且在10 mM BAPTA存在下减少。突触前钙电流的便利化可能有助于短期便利的递质释放，观察时量子输出低。或者，它可以抵消有助于突触抑制的过程。
1. To study use-dependent changes in the presynaptic Ca2+ influx and their contribution to transmitter release, we made simultaneous voltage clamp recordings from presynaptic terminals (the calyces of Held) and postsynaptic cells (the principal cells of the medial nucleus of the trapezoid body) in slices of the rat auditory brainstem.2. Following a short (2 ms) prepulse to 0 mV, calcium channels opened faster during steps to negative test potentials. During trains of action potential waveforms the Ca2+ influx per action potential increased. At the same time, however, the amplitude of the EPSCs decreased.3. The facilitation of the calcium currents appeared to depend on a build-up of intracellular Ca2+, since its magnitude was proportional to the Ca2+ influx and it was reduced in the presence of 10 mM BAPTA.4. Facilitation of the presynaptic calcium currents may contribute to short-term facilitation of transmitter release, observed when quantal output is low. Alternatively it may counteract processes that contribute to synaptic depression.