Developmental Profile of Ion Channel Specializations in the Avian Nucleus Magnocellularis.

Developmental Profile of Ion Channel Specializations in the Avian Nucleus Magnocellularis.
复制标题

DOI:
10.3389/fncel.2016.00080
复制
发表时间:
2016
影响因子:
5.3
通讯作者:
Sanchez JT
Sanchez JT
中科院分区:
医学2区
文献类型:
--
作者:
Hong H;Rollman L;Feinstein B;Sanchez JT

文献摘要

被引文献

相似文献

超快且时间精确的动作电位 (AP) 是听觉脑干神经元的生物物理特化;编码声音定位和通信线索所需的属性。这些专业化的基础是电压依赖性钾 (KV) 和钠 (NaV) 离子通道。在这里,我们描述了这些离子通道的功能发育,并量化了它们如何影响鸟类耳蜗大细胞核 (NM) 的 AP 特性。我们报告说,发育后期的 NM 神经元(胚胎 [E] 天 19-21)生成快速 AP,能够可靠地锁相到 75 Hz 的正弦输入。相比之下,早期发育的神经元 (<E12) 具有较慢且不太可靠的 AP,优先以较低频率 (5-10 Hz) 发射。随着发育,NM神经元的膜时间常数变得更快,而输入电阻和电容降低。输入电阻的变化是由于 KV 电流从 E10 到 E21 增加了 2 倍,并且当高压激活钾 (K+HVA) 通道被阻断时,所有年龄段的 AP 都明显变慢。这对于早期发育的神经元最为明显,其中 K+HVA 电流的比率约占总 KV 响应的 85%。对于发育晚期的神经元,该比率下降至约 50%,表明低电压激活钾 (K+LVA) 通道的发育上调。事实上,K+LVA 的阻断消除了剩余电流并增加了晚期发育神经元的神经兴奋性。我们还报告了 NaV 电流的振幅、动力学和电压依赖性的发展变化。对于早期发育的神经元,NaV 电流幅度的增加是由于通道密度所致,而对于晚期发育的神经元,通道电导占主导地位。从 E10 到 E21,NaV 通道电流变得更快,但电压依赖性有所不同;早期发育的神经元 (<E16) 具有相似的 NaV 通道失活电压,而晚期发育的 NM 神经元 (>E19) 含有在更负电压下失活的 NaV 通道,这表明 NaV 通道亚型发生了变化。总而言之,我们的结果表明,为了在鸟类 NM 中开发快速、可靠的 AP,被动和主动离子通道特性的细化操作是不同的。
Ultrafast and temporally precise action potentials (APs) are biophysical specializations of auditory brainstem neurons; properties necessary for encoding sound localization and communication cues. Fundamental to these specializations are voltage dependent potassium (KV) and sodium (NaV) ion channels. Here, we characterized the functional development of these ion channels and quantified how they shape AP properties in the avian cochlear nucleus magnocellularis (NM). We report that late developing NM neurons (embryonic [E] days 19–21) generate fast APs that reliably phase lock to sinusoidal inputs at 75 Hz. In contrast, early developing neurons (<E12) have slower and less reliable APs that preferentially fire to lower frequencies (5–10 Hz). With development, the membrane time constant of NM neurons became faster, while input resistance and capacitance decreased. Change in input resistance was due to a 2-fold increase in KV current from E10 to E21 and when high-voltage activated potassium (K+HVA) channels were blocked, APs for all ages became significantly slower. This was most evident for early developing neurons where the ratio of K+HVA current accounted for ~85% of the total KV response. This ratio dropped to ~50% for late developing neurons, suggesting a developmental upregulation of low-voltage activated potassium (K+LVA) channels. Indeed, blockade of K+LVA eliminated remaining current and increased neural excitability for late developing neurons. We also report developmental changes in the amplitude, kinetics and voltage dependence of NaV currents. For early developing neurons, increase in NaV current amplitude was due to channel density while channel conductance dominated for late developing neurons. From E10 to E21, NaV channel currents became faster but differed in their voltage dependence; early developing neurons (<E16) had similar NaV channel inactivation voltages while late developing NM neurons (>E19) contained NaV channels that inactivate at more negative voltages, suggesting alterations in NaV channel subtypes. Taken together, our results indicate that the refinement of passive and active ion channel properties operate differentially in order to develop fast and reliable APs in the avian NM.