High safety factor for action potential conduction along axons but not dendrites of cultured hippocampal and cortical neurons
High safety factor for action potential conduction along axons but not dendrites of cultured hippocampal and cortical neurons
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DOI：
10.1152/jn.1998.80.4.2089
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发表时间：
1998-10-01
影响因子：
2.5
通讯作者：
Murphy, TH
中科院分区：
文献类型：
--
作者：
Mackenzie, PJ;Murphy, TH
通过结合钙离子成像和电流钳记录，我们先前报道了在培养的皮质神经元中可以可靠地观察到动作电位(AP)从胞体到轴突终末的传导。为了扩展这些研究，我们评估了Na+AP引起的钙内流作为AP传导的标志，以期在降低传导安全系数的条件下探索轴突和树突兴奋性的机制。正如预期的那样，将细胞外Na+浓度从150降至接近60 mM时，记录在胞体内的AP的幅度降低，但令人惊讶的是，通过测量Ca~(2+)瞬变来监测，并未影响轴突传导。此外，尽管AP波幅有类似的降低，但稀释(20 NM)河豚毒素(TTX)仍可观察到可靠的轴突传导。相反，在低Na+时，沿树突测得的钙瞬变明显减少，尽管仍受河豚毒素敏感的Na+通道的调节。树突状动作电位诱发的钙瞬变在20 nM河豚毒素中也明显减少。这些数据进一步证明，强可兴奋轴突与弱可兴奋树突在功能上是分开的。我们的结论是，神经递质或重复放电对Na+电流或膜电位的调制更有可能影响AP产生前的神经元放电，而不是信号传播到轴突终末。相反，枝晶中反向传播AP的安全系数相对较低，这表明Na+电流调制效应更强。
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 similar to 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.