Amplification of synaptic current by persistent sodium conductance in apical dendrite of neocortical neurons.
Amplification of synaptic current by persistent sodium conductance in apical dendrite of neocortical neurons.
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新皮质神经元顶端树突中持续钠电导放大突触电流。
DOI：
10.1152/jn.1995.74.5.2220
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Crill,WE
中科院分区：
文献类型：
--
作者：
Schwindt,PC;Crill,WE
1. 通过检查特定通道阻断剂对顶端树突远端谷氨酸离子电渗疗法期间到达体细胞的电流的影响，证明了新皮质锥体神经元树突中电压门控通道放大突触电流的证据。 2. 树突状非失活 Na+ 通道与传输电流的电压依赖性放大有关，因为它维持 > 1 秒，并且河豚毒素 (TTX) 消除了大部分这种放大。 3. N-甲基-D-天冬氨酸（NMDA）谷氨酸受体的特异性阻断剂降低了所有电位下谷氨酸诱发电流的幅度，并且还减少了电压依赖性增强的非TTX敏感成分。无论 NMDA 通道是否被阻断，TTX 的效果都是相同的。 4. 我们得出结论，新皮质神经元的顶端树突中存在持续的 Na+ 电导。它与突触位点的 NMDA 电导一起提供了一种对紧张性、兴奋性突触输入进行分级、电压依赖性放大的机制。这种放大导致强直兴奋电流比被动树突更有效地传输到体细胞。
1. Evidence for amplification of synaptic current by voltage-gated channels in dendrites of neocortical pyramidal neurons was demonstrated by examining the effect of specific channel blocking agents on the current arriving at the soma during iontophoresis of glutamate at a distal site on the apical dendrite. 2. Dendritic noninactivating Na+ channels were implicated in this voltage-dependent amplification of the transmitted current because it was maintained for > 1 s and because tetrodotoxin (TTX) eliminated much of this amplification. 3. Specific blockers of N-methyl-D-aspartate (NMDA) glutamate receptors reduced the amplitude of the glutamate-evoked current at all potentials and also reduced the non-TTX-sensitive component of voltage-dependent augmentation. The effects of TTX were identical whether or not NMDA channels were blocked. 4. We conclude that a persistent Na+ conductance exists in the apical dendrite of neocortical neurons. Together with the NMDA conductance at the synaptic site it provides a mechanism for the graded, voltage-dependent amplification of tonic, excitatory synaptic input. This amplification results in much more effective transmission of tonic excitatory current to the soma than would occur in a passive dendrite.