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首页> 外文期刊>Journal of Neurophysiology >Function of NMDA receptors and persistent sodium channels in a feedback pathway of the electrosensory system.
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Function of NMDA receptors and persistent sodium channels in a feedback pathway of the electrosensory system.

机译：NMDA受体和持续钠通道在电传感系统的反馈路径中的功能。

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Voltage-dependent amplification of ionotropic glutamatergic excitatory postsynaptic potentials (EPSPs) can, in many vertebrate neurons, be due either to the intrinsic voltage dependence of N-methyl-D-aspartate (NMDA) receptors, or voltage-dependent persistent sodium channels expressed on postsynaptic dendrites or somata. In the electrosensory lateral line lobe (ELL) of the gymnotiform fish Apteronotus leptorhynchus, glutamatergic inputs onto pyramidal cell apical dendrites provide a system where both amplification mechanisms are possible. We have now examined the roles for both NMDA receptors and sodium channels in the control of EPSP amplitude at these synapses. An antibody specific for the A. leptorhynchus NR1 subunit reacted strongly with ELL pyramidal cells and were particularly abundant in the spines of pyramidal cell apical dendrites. We have also shown that NMDA receptors contributed strongly to the late phase of EPSPs evoked by stimulation of the feedback fibers terminating on the apical dendritic spines; further, these EPSPs were voltage dependent. Blockade of NMDA receptors did not, however, eliminate the voltage dependence of these EPSPs. Blockade of somatic sodium channels by local somatic ejection of tetrodotoxin (TTX), or inclusion of QX314 (an intracellular sodium channel blocker) in the recording pipette, reduced the evoked EPSPs and completely eliminated their voltage dependence. We therefore conclude that, in the subthreshold range, persistent sodium currents are the main contributor to voltage-dependent boosting of EPSPs, even when they have a large NMDA receptor component.
机译：在许多脊椎动物神经元中，离子型谷氨酸能兴奋性突触后电位（EPSPs）的电压依赖性扩增可能是由于N-甲基-D-天冬氨酸（NMDA）受体的内在电压依赖性，或者是在突触后树突或躯体。在裸露于圆线形的鱼Apteronotus leptorhynchus的电感应侧线叶（ELL）中，向锥体细胞顶端树突的谷氨酸能输入提供了一种系统，其中两种扩增机制都是可能的。现在我们已经检查了NMDA受体和钠通道在这些突触中EPSP振幅控制中的作用。细支气管镰刀菌NR1亚基特异的抗体与ELL锥体细胞强烈反应，在锥体细胞顶突的棘突中特别丰富。我们还表明，NMDA受体通过刺激终止于顶端树突棘的反馈纤维而对EPSP的晚期起重要作用。此外，这些EPSP取决于电压。但是，NMDA受体的阻断并不能消除这些EPSP的电压依赖性。通过河豚毒素（TTX）的局部体细胞喷射或在记录移液管中包含QX314（一种细胞内钠通道阻滞剂）来阻断体钠通道，可减少诱发的EPSP，并完全消除其电压依赖性。因此，我们得出的结论是，即使在亚阈值范围内，持续的钠电流也具有较大的NMDA受体成分，它们仍是EPSP电压依赖性升压的主要因素。

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