Dutia M B, Johnston A R
Department of Physiology, Medical School, Edinburgh, UK.
Exp Brain Res. 1998 Jan;118(2):148-54. doi: 10.1007/s002210050266.
The postnatal maturation of medial vestibular nucleus (MVN) neurones was examined in slices of the dorsal brainstem prepared from balb/c mice at specific stages during the first postnatal month. Using spike-shape averaging to analyse the intracellularly recorded action potentials and after-hyperpolarizations (AHPs) in each cell, all the MVN neurones recorded in the young adult (postnatal day 30; P30) mouse were shown to have either a single deep AHP (type A cells), or an early fast and a delayed slow AHP (type B cells). The relative proportions of the two subtypes were similar to those in the young adult rat. At P5, all the MVN cells recorded showed immature forms of either the type A or the type B action potential shape. Immature type A cells had broad spontaneous spikes, and the characteristic single AHP was small in amplitude. Immature type B cells had somewhat narrower spontaneous spikes that were followed by a delayed, apamin-sensitive AHP. The delayed AHP was separated from the repolarisation phase of the spike by a period of isopotentiality. Over the period P10-P15, the mean resting potentials of the MVN cells became more negative, their action potential fall-times became shorter, the single AHP in type A cells became deeper, and the early fast AHP appeared in type B cells. Until P15 cells of varying degrees of electrophysiological maturity were found in the MVN but by P30 all MVN cells recorded were typical adult type A or type B cells. Exposure to the selective blocker of SK-type Ca-activated K channels, apamin (0.3 microM), induced depolarising plateaux and burst firing in immature type B cells at rest. The duration of the apamin-induced bursts and the spike frequency during the bursts were reduced but not abolished after blockade of Ca channels in Ca-free artificial cerebrospinal fluid containing Cd2+. By contrast, in mature type B cells at rest apamin selectively abolished the delayed slow AHP but did not induce bursting activity. Apamin had no effect on the action potential shape of immature type A cells. These data show that the apamin-sensitive I(AHP) is one of the first ionic conductances to appear in type B cells, and that it plays an important role in regulating the intrinsic rhythmicity and excitability of these cells.
在出生后第一个月的特定阶段，从Balb/c小鼠制备的背侧脑干切片中，研究了内侧前庭核（MVN）神经元的产后成熟情况。使用尖峰形状平均法分析每个细胞内记录的动作电位和超极化后电位（AHPs），发现在成年小鼠（出生后第30天；P30）中记录的所有MVN神经元都有单个深AHPs（A型细胞）或早期快速和延迟缓慢AHPs（B型细胞）。这两种亚型的相对比例与成年大鼠相似。在P5时，记录的所有MVN细胞均显示出A型或B型动作电位形状的不成熟形式。不成熟的A型细胞具有宽的自发尖峰，特征性的单个AHPs幅度较小。不成熟的B型细胞具有稍窄的自发尖峰，随后是延迟的、对蜂毒明肽敏感的AHPs。延迟的AHPs与尖峰的复极化阶段由一段等电位期隔开。在P10 - P15期间，MVN细胞的平均静息电位变得更负，其动作电位下降时间变短，A型细胞中的单个AHPs变得更深，B型细胞中出现早期快速AHPs。直到P15，在MVN中发现了不同程度电生理成熟的细胞，但到P30时，记录的所有MVN细胞都是典型的成年A型或B型细胞。暴露于SK型钙激活钾通道的选择性阻断剂蜂毒明肽（0.3 microM）会在静息状态下的不成熟B型细胞中诱导去极化平台和爆发性放电。在含有Cd2+的无钙人工脑脊液中阻断钙通道后，蜂毒明肽诱导的爆发持续时间和爆发期间的尖峰频率降低但未消除。相比之下，在静息状态下的成熟B型细胞中，蜂毒明肽选择性地消除了延迟缓慢的AHPs，但未诱导爆发活动。蜂毒明肽对不成熟A型细胞的动作电位形状没有影响。这些数据表明，对蜂毒明肽敏感的I(AHP)是最早出现在B型细胞中的离子电导之一，并且它在调节这些细胞的内在节律性和兴奋性方面起着重要作用。
