Bourque C W, Brown D A, Renaud L P
J Physiol. 1986 Jun;375:573-86. doi: 10.1113/jphysiol.1986.sp016134.
The occurrence and ionic basis of prolonged plateau depolarizations were studied during intracellular recordings obtained from thirty-nine supraoptic nucleus (s.o.n.) neurosecretory neurones in perfused explants of rat hypothalamus. Replacement of Ca2+ by Ba2+ in the perfusion media enhanced the shoulder on the repolarization phase of the action potentials in all of eleven cells tested. In Ba2+, spike durations increased as the holding membrane potential was made more positive, resulting in plateaux lasting up to 100 s. These plateaux were characterized by a sustained but slowly decaying absolute potential near 0 mV from which there appeared frequent spontaneous hyperpolarizing transients. A membrane resistance decrease of more than 50% was observed at the onset of a plateau, with gradual restoration during the plateau. Injection of Cs+ into twenty-one cells abolished the spike frequency adaptation and after-hyperpolarization associated with current-evoked bursts of action potentials. Mean spike duration after Cs+ injection increased from 2.5 +/- 0.3 ms to 68 +/- 9 ms (S.E. of mean). Addition of 4-5 mM-tetraethylammonium (TEA) to the perfusion media further increased the spike duration of nine Cs+-injected cells to 320 +/- 70 ms. No further increase could be obtained by doubling the concentration of TEA and/or by the addition of 0.2-0.5 mM-4-aminopyridine to the media. Although spike duration was greatly prolonged during such extensive blockade of K+ channels, plateau potentials lasting for longer than 1 s were observed only when Ba2+ was eventually added to the perfusion media. The special property of Ba2+ that leads to the formation of plateau potentials in s.o.n. neurones is therefore not restricted to its ability to reduce K+ conductances but may reside in its reduced effectiveness as a mediator of Ca2+-dependent inactivation of Ca2+ channels. Injection of Cs+ into s.o.n. neurones increased the slope of their current-voltage relationship below -60 mV from 148 +/- 15 to 257 +/- 41 M omega (S.E. of mean) and eliminated the outward rectification present at potentials above -60 mV. K+ currents are presumably active near the resting potential of these cells. Addition of Ba2+ to the perfusion media revealed a Cd2+-sensitive inward rectification above but not below ca. -55 mV. A slowly inactivating Ba2+ current is therefore carried through Ca2+ channels at potentials above -55 mV.(ABSTRACT TRUNCATED AT 400 WORDS)
在从大鼠下丘脑灌流外植体的39个视上核(s.o.n.)神经分泌神经元获得的细胞内记录过程中,研究了延长的平台期去极化的发生及其离子基础。在灌注介质中用Ba2+替代Ca2+增强了所有11个受试细胞动作电位复极化阶段的肩部。在Ba2+中,随着膜电位保持得更正,动作电位持续时间增加,导致平台期持续长达100秒。这些平台期的特征是在接近0 mV处有持续但缓慢衰减的绝对电位,从中出现频繁的自发超极化瞬变。在平台期开始时观察到膜电阻下降超过50%,在平台期内逐渐恢复。向21个细胞注射Cs+消除了与电流诱发的动作电位爆发相关的动作电位频率适应性和后超极化。注射Cs+后的平均动作电位持续时间从2.5±0.3毫秒增加到68±9毫秒(平均值的标准误)。向灌注介质中添加4-5 mM四乙铵(TEA)进一步将9个注射Cs+的细胞的动作电位持续时间增加到320±70毫秒。将TEA浓度加倍和/或向介质中添加0.2-0.5 mM 4-氨基吡啶均不能使动作电位持续时间进一步增加。尽管在如此广泛的K+通道阻断期间动作电位持续时间大大延长,但仅当最终向灌注介质中添加Ba2+时才观察到持续超过1秒的平台期电位。因此,导致s.o.n.神经元中平台期电位形成的Ba2+的特殊性质不仅限于其降低K+电导的能力,还可能在于其作为Ca2+通道钙依赖性失活介质的有效性降低。向s.o.n.神经元注射Cs+使低于-60 mV的电流-电压关系斜率从148±15增加到257±41 MΩ(平均值的标准误),并消除了高于-60 mV电位时存在的外向整流。K+电流可能在这些细胞的静息电位附近活跃。向灌注介质中添加Ba2+揭示了在约-55 mV以上但在其以下不存在对Cd2+敏感的内向整流。因此,在高于-55 mV的电位下,通过Ca2+通道携带缓慢失活的Ba2+电流。(摘要截短于400字)