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首页> 外文期刊>Journal of Neurophysiology >Voltage-gated sodium channels shape subthreshold EPSPs in layer 5 pyramidal neurons from rat prefrontal cortex.
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Voltage-gated sodium channels shape subthreshold EPSPs in layer 5 pyramidal neurons from rat prefrontal cortex.

机译：电压门控钠通道在大鼠前额叶皮层的第5层锥体神经元中形成亚阈值EPSP。

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摘要

The role of voltage-dependent channels in shaping subthreshold excitatory postsynaptic potentials (EPSPs) in neocortical layer 5 pyramidal neurons from rat medial prefrontal cortex (PFC) was investigated using patch-clamp recordings from visually identified neurons in brain slices. Small-amplitude EPSPs evoked by stimulation of superficial layers were not affected by the N-methyl-D-aspartate receptor antagonist D-2-amino-5-phosphonopentanoic acid but were abolished by the AMPA receptor antagonist 6-cyano-7-nitroquinoxalene-2,3-dione, suggesting that they were primarily mediated by AMPA receptors. AMPA receptor-mediated EPSPs (AMPA-EPSPs) evoked in the apical dendrites were markedly enhanced, or increased in peak and duration, at depolarized holding potentials. Enhancement of AMPA-EPSPs was reduced by loading the cells with lidocaine N-ethylbromide (QX-314) and by local application of the Na(+) channel blocker tetrodotoxin (TTX) to the soma but not to the middle/proximal apical dendrite. In contrast, blockade of Ca(2+) channels by co-application of Cd(2+) and Ni(2+) to the soma or apical dendrite did not affect the AMPA-EPSPs. Like single EPSPs, EPSP trains were shaped by Na(+) but not Ca(2+) channels. EPSPs simulated by injecting synaptic-like current into proximal/middle apical dendrite (simEPSPs) were enhanced at depolarized holding potentials similarly to AMPA-EPSPs. Extensive blockade of Ca(2+) channels by bath application of the Cd(2+) and Ni(2+) mixture had no effects on simEPSPs, whereas bath-applied TTX removed the depolarization-dependent EPSP amplification. Inhibition of K(+) currents by 4-aminopyridine (4-AP) and TEA increased the TTX-sensitive EPSP amplification. Moreover, strong inhibition of K(+) currents by high concentrations of 4-AP and TEA revealed a contribution of Ca(2+) channels to EPSPs that, however, seemed to be dependent on Na(+) channel activation. Our results indicate that in layer 5 pyramidal neurons from PFC, Na(+), and K(+) voltage-gated channels shape EPSPs within the voltage range that is subthreshold for somatic action potentials.
机译：电压依赖性通道在塑造大鼠前额内侧皮层（PFC）的新皮层5锥体神经元的阈下兴奋性突触后突触电位（EPSPs）中的作用，使用视觉识别的大脑切片神经元的膜片钳记录进行了研究。 N-甲基-D-天门冬氨酸受体拮抗剂D-2-氨基-5-膦基戊酸不影响通过表层刺激引起的小幅度EPSP，而AMPA受体拮抗剂6-氰基-7-硝基喹喔啉-则消除了小振幅EPSP。 2,3-二酮，表明它们主要由AMPA受体介导。在去极化的保持电位下，在根尖树突中诱发的AMPA受体介导的EPSP（AMPA-EPSP）显着增强，或在峰和持续时间内增加。通过向细胞中加载利多卡因N-乙基溴化物（QX-314）并通过将Na（+）通道阻滞剂河豚毒素（TTX）局部应用到躯体而不是中/近端根尖树突，可以减少AMPA-EPSP的增强。相比之下，通过将Cd（2+）和Ni（2+）共同应用到体细胞或顶端树突来阻断Ca（2+）通道不会影响AMPA-EPSPs。像单个EPSP一样，EPSP火车的形状是Na（+），而不是Ca（2+）通道。与AMPA-EPSP相似，通过在近端/中间根尖突（simEPSPs）中注入突触样电流来模拟的EPSP在去极化保持电位下得到增强。通过浴应用Cd（2+）和Ni（2+）混合物对Ca（2+）通道的广泛阻滞对simEPSPs没有影响，而应用浴的TTX去除了去极化依赖性EPSP扩增。 4-氨基吡啶（4-AP）和TEA抑制K（+）电流增加了TTX敏感的EPSP扩增。此外，高浓度的4-AP和TEA对K（+）电流的强烈抑制作用揭示了Ca（2+）通道对EPSP的贡献，然而，这似乎取决于Na（+）通道的激活。我们的结果表明，在来自PFC的第5层锥体神经元，Na（+）和K（+）电压门控通道中，EPSP在低于躯体动作电位的阈值电压范围内成形。

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