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培养的海马体和皮层神经元的轴突而非树突在动作电位传导方面具有高安全系数。

High safety factor for action potential conduction along axons but not dendrites of cultured hippocampal and cortical neurons.

作者信息

Mackenzie P J, Murphy T H

机构信息

Kinsmen Laboratory of Neurological Research, Departments of Psychiatry and Physiology, University of British Columbia, Vancouver V6T 1Z3, Canada.

出版信息

J Neurophysiol. 1998 Oct;80(4):2089-101. doi: 10.1152/jn.1998.80.4.2089.

DOI:10.1152/jn.1998.80.4.2089
PMID:9772263
Abstract

By using a combination of Ca2+ imaging and current-clamp recording, we previously reported that action potential (AP) conduction is reliably observed from the soma to axonal terminals in cultured cortical neurons. To extend these studies, we evaluated Ca2+ influx evoked by Na+ APs as a marker of AP conduction under conditions that are expected to lower the conduction safety factor to explore mechanisms of axonal and dendritic excitability. As expected, reducing the extracellular Na+ concentration from 150 to approximately 60 mM decreased the amplitude of APs recorded in the soma but surprisingly did not influence axonal conduction, as monitored by measuring Ca2+ transients. Furthermore, reliable axonal conduction was observed in dilute (20 nM) tetrodotoxin (TTX), despite a similar reduction in AP amplitude. In contrast, the Ca2+ transient measured along dendrites was markedly reduced in low Na+, although still mediated by TTX-sensitive Na+ channels. Dendritic action-potential evoked Ca2+ transients were also markedly reduced in 20 nM TTX. These data provide further evidence that strongly excitable axons are functionally compartmentalized from weakly excitable dendrites. We conclude that modulation of Na+ currents or membrane potential by neurotransmitters or repetitive firing is more likely to influence neuronal firing before AP generation than the propagation of signals to axonal terminals. In contrast, the relatively low safety factor for back-propagating APs in dendrites would suggest a stronger effect of Na+ current modulation.

摘要

通过结合使用钙离子成像和电流钳记录技术,我们之前报道过在培养的皮层神经元中能够可靠地观察到动作电位(AP)从胞体传导至轴突终末。为了拓展这些研究,我们将钠离子动作电位诱发的钙离子内流作为动作电位传导的一个标志物进行评估,研究条件设定为降低传导安全系数,以此来探索轴突和树突兴奋性的机制。正如预期的那样,将细胞外钠离子浓度从150 mM降低至约60 mM会使胞体记录到的动作电位幅度减小,但令人惊讶的是,通过测量钙离子瞬变发现这并未影响轴突传导。此外,在稀释的(20 nM)河豚毒素(TTX)中也观察到了可靠的轴突传导,尽管动作电位幅度也有类似程度的降低。相比之下,在低钠离子浓度条件下,沿树突测量的钙离子瞬变明显降低,尽管其仍由TTX敏感的钠离子通道介导。在20 nM TTX中,树突动作电位诱发的钙离子瞬变也明显降低。这些数据进一步证明,强兴奋性的轴突在功能上与弱兴奋性的树突是分隔开的。我们得出结论,神经递质或重复放电对钠离子电流或膜电位的调节,在动作电位产生之前比信号向轴突终末的传播更有可能影响神经元的放电。相比之下,树突中反向传播动作电位相对较低的安全系数表明钠离子电流调节的作用更强。

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