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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >CALCIUM REGULATION OF A SLOW POST-SPIKE HYPERPOLARIZATION IN VAGAL AFFERENT NEURONS
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CALCIUM REGULATION OF A SLOW POST-SPIKE HYPERPOLARIZATION IN VAGAL AFFERENT NEURONS

机译：迷走神经传入后缓慢的峰后超极化的钙调节

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摘要

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 Ca~2+-dependen K~+ current. This current produces a post-spike hyperpolarization (AHPslow) 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 <0.1 to >10 Hz. After a single action potential, the AHP_slow in nodose neurons displays a slow rise time to peak (0.3-0.5s) and a long duration (3-15s). The slow kinetics of the AHP_slow are due, in part, to Ca~2+ discharge from an intracellular Ca~2+-induced Ca~2+ release (CICR) pool. Action potential-evoked Ca~2+ influx via either L or N type Ca(2+) channels triggers CICR. Surprisingly, although L type channels generate 60/100 of action potential-induced CICR, only Ca~2+ influx through N type Ca~2+ 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 Ca~2+ channels and AHP_slow potassium channels. Such an anatomical relation might be particularly beneficial for modulation of spike-frequency adaptation in vagal afferent neurons.
机译：不同类别的钾通道的激活会极大地影响神经元放电的频率和模式。在迷走神经传入神经元（结节神经节神经元）的亚群中，冲动活动的模式可以通过依赖Ca〜2 +的K〜+电流有效地调节。该电流产生了尖峰后超极化（AHPslow），其在调节膜兴奋性中起关键作用，并负责这些神经元中的尖峰频率调节。许多内源性自发性类胡萝卜素（例如组胺，5-羟色胺，前列腺素和缓激肽）对AHP_slow的抑制作用导致迷走神经传入神经元的放电频率从<0.1增至> 10 Hz。单个动作电位后，结节神经元中的AHP_slow显示出缓慢的峰值上升时间（0.3-0.5s）和长的持续时间（3-15s）。 AHP_slow的缓慢动力学部分是由于细胞内Ca〜2 +诱导的Ca〜2 +释放（CICR）库中Ca〜2 +的释放。通过L型或N型Ca（2+）通道引起的动作电位诱发的Ca〜2 +流入触发CICR。出人意料的是，尽管L型通道产生60/100的动作电位诱导的CICR，但是只有通过N型Ca〜2 +通道的Ca〜2 +流入才能触发依赖CICR的AHP_slow。这些观察结果表明内质网ryanodine受体与质膜N型Ca〜2 +通道和AHP_slow钾通道之间存在紧密的物理接近。这样的解剖关系对于迷走神经传入神经元的峰频率适应的调制可能特别有益。

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