Mechanisms underlying the activity-dependent regulation of locomotor network performance by the Na+ pump.
Mechanisms underlying the activity-dependent regulation of locomotor network performance by the Na+ pump.
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DOI：
10.1038/srep16188
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发表时间：
2015-11-06
影响因子：
4.6
通讯作者：
Sillar KT
中科院分区：
文献类型：
--
作者：
Zhang HY;Picton L;Li WC;Sillar KT
神经网络输出的活动依赖性改变通常由神经递质释放和/或膜电导的变化引起。在爪蟾蝌蚪中，脊髓运动网络输出被Na+泵电流增加介导的超低后超极化（usAHP）所适应。在这里，我们系统地探讨了两次游泳之间的间隔如何影响第二次发作，它比第一次发作更短，更慢。我们发现，除了兴奋性下降中间神经元（dINs）外，脊髓节律性神经元在第二次发作时的放电可靠性较低。钠/质子反向转运蛋白莫能菌素可增强钠离子泵功能，与短间隔游泳产生相似的效果。超阈脉冲诱发的usAHP降低了游泳过程中神经元放电的可靠性。它还增加了尖峰的阈值电流，并在列车的第一个尖峰中引入了延迟，但没有降低随后的发射频率。沃巴因或零钾盐水消除了这种延迟，从而消除了usAHP。我们提出的证据表明，脊髓CPG神经元中存在a型K+电流，该电流通过去极化和超极化灭活来灭活，并解释了延长的延迟。我们得出结论，usAHP通过膜超极化和增强a电流去失活来减弱神经元对兴奋性网络输入的反应。
Activity-dependent modification of neural network output usually results from changes in neurotransmitter release and/or membrane conductance. In Xenopus frog tadpoles, spinal locomotor network output is adapted by an ultraslow afterhyperpolarization (usAHP) mediated by an increase in Na+ pump current. Here we systematically explore how the interval between two swimming episodes affects the second episode, which is shorter and slower than the first episode. We find the firing reliability of spinal rhythmic neurons to be lower in the second episode, except for excitatory descending interneurons (dINs). The sodium/proton antiporter, monensin, which potentiates Na+ pump function, induced similar effects to short inter-swim intervals. A usAHP induced by supra-threshold pulses reduced neuronal firing reliability during swimming. It also increased the threshold current for spiking and introduced a delay to the first spike in a train, without reducing subsequent firing frequency. This delay was abolished by ouabain or zero K+ saline, which eliminate the usAHP. We present evidence for an A-type K+ current in spinal CPG neurons which is inactivated by depolarization and de-inactivated by hyperpolarization, and accounts for the prolonged delay. We conclude that the usAHP attenuates neuronal responses to excitatory network inputs by both membrane hyperpolarization and enhanced de-inactivation of an A-current.