Calcium regulation of a slow post-spike hyperpolarization in vagal afferent neurons
Calcium regulation of a slow post-spike hyperpolarization in vagal afferent neurons
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DOI：
10.1073/pnas.96.14.7650
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发表时间：
1999-07-06
影响因子：
11.1
通讯作者：
Weinreich, D
中科院分区：
文献类型：
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作者：
Cordoba-Rodriguez, R;Moore, KA;Weinreich, D
不同类型的钾通道的激活可以显著影响神经元放电的频率和模式。在迷走神经传入神经元（结状神经节神经元）的亚群，脉冲活动的模式是有效地调制的钙依赖性K+电流。该电流产生后尖峰超极化（AHP（慢）），其在膜兴奋性的调节中起关键作用，并且负责这些神经元中的尖峰频率调节。通过许多内源性autacoid（例如，组胺、5-羟色胺、前列腺素类和缓激肽）导致迷走传入神经元的放电频率从10 Hz增加。在单个动作电位后，结状神经元的AHP（慢）显示缓慢的上升时间（0.3-0.5 s）和较长的持续时间（3-15 s）。AHP的缓慢动力学（缓慢）部分是由于细胞内Ca 2+诱导的Ca 2+释放（CICR）池的Ca 2+放电。动作电位诱发的Ca ~（2+）内流通过L型或N型Ca ~（2+）通道触发CICR。令人惊讶的是，虽然L型通道产生60%的动作电位诱导的CICR，但只有通过N型Ca 2+通道的Ca 2+内流才能触发CICR依赖性AHP（缓慢）。这些观察结果表明，内质网ryanodine受体和质膜N型钙通道和AHP（慢）钾通道之间存在着密切的物理接近。这种解剖关系可能是特别有益的调制迷走神经传入神经元的尖峰频率适应。
Activation of distinct classes of potassium channels can dramatically affect the frequency and the pattern of neuronal firing. In a subpopulation of vagal afferent neurons (nodose ganglion neurons), the pattern of impulse activity is effectively modulated by a Ca2+-dependent K+ current. This current produces a post-spike hyperpolarization (AHP(slow)) that plays a critical role in the regulation of membrane excitability and is responsible for spike-frequency accommodation in these neurons. Inhibition of the AHP(slow) by a number of endogenous autacoids (e.g., histamine, serotonin, prostanoids, and bradykinin) results in an increase in the firing frequency of vagal afferent neurons from 10 Hz. After a single action potential, the AHP(slow) in nodose neurons displays a slow rise time to peak (0.3-0.5 s) and a long duration (3-15 s). The slow kinetics of the AHP(slow) are due, in part, to Ca2+ discharge from an intracellular Ca2+-induced Ca2+ release (CICR) pool. Action potential-evoked Ca2+ influx via either L or N type Ca2+ channels triggers CICR. Surprisingly, although L type channels generate 60% of action potential-induced CICR, only Ca2+ influx through N type Ca2+ channels can trigger the CICR-dependent AHP(slow). These observations suggest that a close physical proximity exists between endoplasmic reticulum ryanodine receptors and plasma membrane N type Ca2+ channels and AHP(slow) potassium channels. Such an anatomical relation might be particularly beneficial for modulation of spike-frequency adaptation in vagal afferent neurons.