Peptidergic counter-regulation of Ca2+- and Na+-dependent K+ currents modulates the shape of action potentials in neurosecretory insect neurons
Peptidergic counter-regulation of Ca2+- and Na+-dependent K+ currents modulates the shape of action potentials in neurosecretory insect neurons
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DOI：
10.1152/jn.00904.2005
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发表时间：
2006-01-01
影响因子：
2.5
通讯作者：
Borst, A
中科院分区：
文献类型：
--
作者：
Wicher, D;Berlau, J;Borst, A
肽能反调节钙和钠依赖性钾电流调节昆虫神经分泌神经元动作电位的形状神经生理学杂志95：311 - 322，2006年。首次发表于2005年9月21日; doi：10.1152/jn.00904.2005。如果神经元表达Ca ~（2+）和Na ~+依赖的K ~+电流（K-Ca和K-Na），则动作电位过程中Ca ~（2+）和Na ~+离子的内流会强烈影响复极和快后超极化（fAHP）。这适用于蟑螂腹背不成对正中神经元（DUMS）。KCa的快速激活主要依赖于P/Q型Ca ~（2+）电流。脂肪动力激素（AKH）-昆虫对应哺乳动物胰高血糖素-动员能量储备，但也调节神经元活动，并导致增强的运动活性。蟑螂AKH I加速了章鱼胺能DUM神经元的尖峰发放并增强了fAHP，并且通常认为来自这些和其他神经元的生物胺的增强释放可能导致一般唤醒。AKH I调节电压门控Na+和P/Q型Ca ~（2+）电流以及背景Ca ~（2+）电流。P/Q型Ca ~（2+）电流的上调使K-Ca电流增加，而Na ~+电流的失活则使K-Na电流降低。我们量化的Hodgkin-Huxley模型的离子电流的变化，并模拟DUM神经元的活动。P/Q型Ca ~（2+）和KCa ~（2+）电流的上调增强了心肌细胞的超极化，但对峰电位的影响较弱。Na+和K-Na电流的下调降低超极化和轻微加速尖峰。叠加这些调制产生的fAHP增加，而尖峰频率保持不变。只有当起搏Ca 2+背景电流的上调被包括在模拟调制的模型再现实验观察到AKH-I诱导的变化。这种双重效应的可能的生理相关性进行了讨论方面的发射器释放和突触整合。
Peptidergic counter-regulation of Ca2+- and Na+-dependent K+ currents modulates the shape of action potentials in neurosecretory insect neurons. J Neurophysiol 95: 311 - 322, 2006. First published September 21, 2005; doi:10.1152/jn.00904.2005. Influx of Ca2+ and Na+ ions during an action potential can strongly affect the repolarization and the fast afterhyperpolarization (fAHP) if a neuron expresses Ca2+- and Na+-dependent K+ currents (K-Ca and K-Na). This applies to cockroach abdominal dorsal unpaired median neurons (DUMs). Here the rapid activation of KCa depends mainly on the P/Q-type Ca2+ current. Adipokinetic hormones (AKHs)-insect counterparts to mammalian glucagon - mobilize energy reserves but also modulate neuronal activity and lead to enhanced locomotor activity. Cockroach AKH I accelerates spiking and enhances the fAHP of octopaminergic DUM neurons, and it is generally held that enhanced release of the biogenic amine from these and other neurons may lead to general arousal. AKH I modulates the voltage-gated Na+ and P/Q-type Ca2+ current and the background Ca2+ current. Upregulation of P/Q-type Ca2+ current increases the K-Ca current, whereas enhanced inactivation of Na+ current decreases the K-Na current. We quantified the hormone-induced changes in ion currents in terms of Hodgkin-Huxley models and simulated the resulting activity of DUM neurons. Upregulation of P/Q-type Ca2+ and KCa current enhanced the hyperpolarization but had a weak effect on spiking. Downregulation of Na+ and K-Na current decreased hyperpolarization and slightly accelerated spiking. Superposition of these modulations produced an increase in fAHP while the spike frequency remained unchanged. Only when the upregulation of the pacemaking Ca2+ background current was included in the simulated modulation the model reproduced the experimentally observed AKH-I-induced changes. The possible physiological relevance of this dual effect is discussed in respect to transmitter release and synaptic integration.