Action potentials clustered into high-frequency bursts play distinct roles in neural computations. However, little is known about ionic currents that control the duration and probability of these bursts. We found that, in cartwheel inhibitory interneurons of the dorsal cochlear nucleus, the likelihood of bursts and the interval between their spikelets were controlled by Ca²⁺ acting across two nanodomains, one between plasma membrane P/Q Ca²⁺ channels and endoplasmic reticulum (ER) ryanodine receptors and another between ryanodine receptors and large-conductance, voltage- and Ca²⁺-activated K⁺ (BK) channels. Each spike triggered Ca²⁺-induced Ca²⁺ release (CICR) from the ER immediately beneath somatic, but not axonal or dendritic, plasma membrane. Moreover, immunolabeling demonstrated close apposition of ryanodine receptors and BK channels. Double-nanodomain coupling between somatic plasma membrane and hypolemmal ER cisterns provides a unique mechanism for rapid control of action potentials on the millisecond timescale.

中文翻译：

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钙通道，Ryanodine受体和BK通道的双纳米域耦合控制着爆炸的产生。

聚集到高频脉冲中的动作电位在神经计算中起着不同的作用。但是，对于控制这些脉冲的持续时间和概率的离子电流知之甚少。我们发现，在耳蜗后侧核的车轮抑制性中间神经元中，爆发的可能性及其小穗之间的间隔受到跨两个纳米域起作用的Ca ^2+的控制，其中一个在质膜P / Q Ca ²⁺通道与内质网之间（ ER）ryanodine受体，另一个在ryanodine受体与大电导，电压和Ca ²⁺激活的K ⁺（BK）通道之间。每个尖峰触发Ca ²⁺诱导的Ca ²⁺在体细胞膜下但不是在轴突或树突状质膜下从ER中释放（CICR）。此外，免疫标记显示了ryanodine受体和BK通道紧密并置。体细胞质膜和下垂的ER储水池之间的双纳米域耦合提供了一种独特的机制，可以在毫秒级的时间尺度上快速控制动作电位。