Calcium stores in hippocampal synaptic boutons mediate short-term plasticity, store-operated Ca2+ entry, and spontaneous transmitter release
Calcium stores in hippocampal synaptic boutons mediate short-term plasticity, store-operated Ca2+ entry, and spontaneous transmitter release
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DOI：
10.1016/s0896-6273(01)00190-8
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发表时间：
2001-01-01
期刊：
影响因子：
16.2
通讯作者：
Fine, A
中科院分区：
文献类型：
--
作者：
Emptage, NJ;Reid, CA;Fine, A
诱发的递质释放取决于钙流入突触纽扣，但调节纽扣钙水平和自发递质释放的机制尚不清楚。为了更好地理解这些过程，我们监测了海马切片培养物中锥体神经元轴突和突触前末端的钙瞬变。动作电位可靠地引起轴突和突触中的钙瞬变。内部存储的钙诱导钙释放 (CICR) 有助于波顿的瞬态和 EPSP 的配对脉冲促进。钙池耗尽会激活钙池操纵的钙通道，影响自发递质释放的频率。 Boutons 显示自发 Ca2+ 瞬变；阻断 CICR 可以降低这些瞬变和自发微型突触事件的频率。因此，自发的递质释放主要是钙介导的，由内部储存的 Ca2+ 释放驱动。 Bouton 商店释放对于短期突触可塑性很重要，也可能有助于长期可塑性。
Evoked transmitter release depends upon calcium influx into synaptic boutons, but mechanisms regulating bouton calcium levels and spontaneous transmitter release are obscure. To understand these processes better, we monitored calcium transients in axons and presynaptic terminals of pyramidal neurons in hippocampal slice cultures. Action potentials reliably evoke calcium transients in axons and boutons. Calcium-induced calcium release (CICR) from internal stores contributes to the transients in boutons and to paired-pulse facilitation of EPSPs. Store depletion activates store-operated calcium channels, influencing the frequency of spontaneous transmitter release. Boutons display spontaneous Ca2+ transients; blocking CICR reduces the frequency of these transients and of spontaneous miniature synaptic events. Thus, spontaneous transmitter release is largely calcium mediated, driven by Ca2+ release from internal stores. Bouton store release is important for short-term synaptic plasticity and may also contribute to long-term plasticity.