Functional dependence of Ca(2+)-activated K+ current on L- and N-type Ca2+ channels: differences between chicken sympathetic and parasympathetic neurons suggest different regulatory mechanisms.
Functional dependence of Ca(2+)-activated K+ current on L- and N-type Ca2+ channels: differences between chicken sympathetic and parasympathetic neurons suggest different regulatory mechanisms.
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Ca(2) 激活的 K 电流对 L 型和 N 型 Ca2 通道的功能依赖性：鸡交感神经元和副交感神经元之间的差异表明了不同的调节机制。
DOI：
10.1073/pnas.91.7.2858
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发表时间：
1994
影响因子：
11.1
通讯作者：
Dryer,SE
中科院分区：
文献类型：
--
作者：
Wisgirda,ME;Dryer,SE
Ca2+离子的内流控制了可兴奋细胞中的许多重要过程，包括Ca（2+）激活的K+通道的门控调节（目前的IK[Ca]）。不同的IK[Ca]通道有助于动作电位波形的调节、脉冲的重复放电和神经递质的分泌。人们认为，大电导IK[Ca]通道必须与Ca2+通道（ICa）紧密共定位，才能被Ca2+内流门控。我们现在报道，IK[Ca]通道可以优先与药理学上不同的电压激活Ca2+通道亚型共定位，这在胚胎鸡交感和副交感神经元中发生不同。通过对胚胎鸡纤毛和交感神经节神经元的穿孔补片全细胞记录，研究了各种二氢吡啶和ω - concontoxin对电压激活的Ca2+电流（ICa）和Ca（2+）激活的K+电流（IK[Ca]）的影响。应用硝苯地平或omega- concontoxin均可使ICa减少40-60%，而应用S-(-)- bay K 8644可增强睫状神经节神经元中的ICa。但应用omega- concontoxin对IK[Ca]几乎没有影响，而硝苯地平和S-(-)- bay k8644分别抑制和增强IK[Ca]。这些结果表明，鸡睫状神经节神经元上的IK[Ca]通道优先偶联l型Ca2+通道，而不是n型Ca2+通道。鸡交感神经细胞也表达对二氢吡啶敏感和对ω -conotoxin敏感的ICa成分。然而，在这些细胞中，应用omega- concontoxin可使IK[Ca]降低40-60%，而硝苯地平可降低IK[Ca]，但仅在细胞亚群中。因此，交感神经元中的IK[Ca]要么与n型Ca2+通道偶联，要么不选择性地与单一Ca（2+）通道亚型偶联。IK[Ca]通道与不同ICa亚型的优先耦合可能是允许选择性调节神经递质释放的机制的一部分。优先偶联也可能对脊椎动物神经元的分化和发育起重要作用。
The influx of Ca2+ ions controls many important processes in excitable cells, including the regulation of the gating of Ca(2+)-activated K+ channels (the current IK[Ca]). Various IK[Ca] channels contribute to the regulation of the action-potential waveform, the repetitive discharge of spikes, and the secretion of neurotransmitters. It is thought that large-conductance IK[Ca] channels must be closely colocalized with Ca2+ channels (ICa) to be gated by Ca2+ influx. We now report that IK[Ca] channels can be preferentially colocalized with pharmacologically distinct subtypes of voltage-activated Ca2+ channel and that this occurs differently in embryonic chicken sympathetic and parasympathetic neurons. The effects of various dihydropyridines and omega-conotoxin on voltage-activated Ca2+ currents (ICa) and Ca(2+)-activated K+ currents (IK[Ca]) were examined by using perforated-patch whole-cell recordings from embryonic chicken ciliary and sympathetic ganglion neurons. Application of nifedipine or omega-conotoxin each caused a 40-60% reduction in ICa, whereas application of S-(-)-BAY K 8644 potentiated ICa in ciliary ganglion neurons. But application of omega-conotoxin had little or no effect on IK[Ca], whereas nifedipine and S-(-)-BAY K 8644 inhibited and potentiated IK[Ca], respectively. These results indicate that IK[Ca] channels are preferentially coupled to L-type, but not to N-type, Ca2+ channels on chicken ciliary ganglion neurons. Chicken sympathetic neurons also express dihydropyridine-sensitive and omega-conotoxin-sensitive components of ICa. However, in those cells, application of omega-conotoxin caused a 40-60% reduction in IK[Ca], whereas nifedipine reduced IK[Ca] but only in a subpopulation of cells. Therefore, IK[Ca] in sympathetic neurons is either coupled to N-type Ca2+ channels or is not selectively coupled to a single Ca(2+)-channel subtype. The preferential coupling of IK[Ca] channels with distinct ICa subtypes may be part of a mechanism to allow for selective modulation of neurotransmitter release. Preferential coupling may also be important for the differentiation and development of vertebrate neurons.