Endogenous calcium buffers regulate fast exocytosis in the synaptic terminal of retinal bipolar cells
Endogenous calcium buffers regulate fast exocytosis in the synaptic terminal of retinal bipolar cells
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DOI：
10.1016/s0896-6273(01)00565-7
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发表时间：
2002-01-03
期刊：
影响因子：
16.2
通讯作者：
Lagnado, L
中科院分区：
文献类型：
--
作者：
Burrone, J;Neves, G;Lagnado, L
添加钙螯合剂可抑制突触处钙触发的胞吐作用，但内源性 Ca2+ 缓冲液的作用尚未经过测试。我们发现，视网膜双极细胞突触末端 80% 的 Ca2+ 结合位点与抑制 Ca2+（敏感 K+ 通道）激活的移动分子相关，其效率相当于 1.2 mM BAPTA。去除这些缓冲液导致持续约 0.5 ms 的 Ca2+ 尾流释放的囊泡数量增加 30 倍，并且快速释放囊泡池 (RRP) 增加 2 倍。 BAPTA 和 EGTA 的作用表明，包含 RRP 的囊泡与 Ca2+ 通道的距离不同。我们认为内源性 Ca2+ 缓冲液通过抑制囊泡向活性区外围的释放来调节 RRP 的大小。
Calcium-triggered exocytosis at the synapse is suppressed by addition of calcium chelators, but the effects of endogenous Ca2+ buffers have not been tested. We find that 80% of Ca2+ binding sites in the synaptic terminal of retinal bipolar cells were associated with mobile molecules that suppressed activation of Ca2+, sensitive K+ channels with an efficiency equivalent to similar to1.2 mM BAPTA. Removing these buffers caused a 30-fold increase In the number of vesicles released by Ca2+ tail currents lasting similar to0.5 ms and a 2-fold increase in the rapidly releasable pool of vesicles (RRP). The effects of BAPTA and EGTA indicate that vesicles comprising the RRP were docked at variable distances from Ca2+ channels. We propose that endogenous Ca2+ buffers regulate the size of the RRP by suppressing the release of vesicles toward the periphery of the active zone.