PROPERTIES OF 2 CALCIUM-ACTIVATED HYPERPOLARIZATIONS IN RAT HIPPOCAMPAL-NEURONS
PROPERTIES OF 2 CALCIUM-ACTIVATED HYPERPOLARIZATIONS IN RAT HIPPOCAMPAL-NEURONS
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DOI：
10.1113/jphysiol.1987.sp016653
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发表时间：
1987-08-01
影响因子：
5.5
通讯作者：
NICOLL, RA
中科院分区：
文献类型：
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作者：
LANCASTER, B;NICOLL, RA
1. 利用切片制备海马CA1锥体细胞的细胞内记录，分析动作电位复极化和动作电位后超极化的药理学敏感性。Ca2+激活后超极化（a.h.p.s）可分为时间为毫秒级的快速超极化和在30度温度下持续数秒的慢速超极化。c . 2。动作电位的复极化对Ca2+通道阻滞剂Cd2+敏感。这种效应与动作电位复极后立即发生的快速a.h.p.阻滞同时发生。缓慢的a.h.p.也被Cd2+阻断。3. 低浓度的K+通道阻滞剂四乙基铵（TEA: 200-500 .mu）。M)，阻断快速a.h.p.，减缓动作电位复极化。低浓度的TEA不影响慢速a.h.p.。4. 动作电位复极和快速a.h.p.对肉毒杆菌毒素也具有可逆性敏感性。该药对慢速a.h.p无作用。在正常记录电解质（KMeSO4）中加入EGTA或BAPTA，可阻止慢速a.h.p.s.的产生。此外，与单独含有KMeSO3或含有EGTA的电极相比，含有bapta的电极刺穿的细胞显示出更宽的动作电位和更低的快速a.h.p.s。6. 缓慢的a.h.p.可以通过去甲肾上腺素、8-溴环AMP或氨基酚来消除。在这些条件下，对快速a.h.p.和动作电位持续时间没有影响。7. 用TEA或CTX （charybdotoxin）阻断快速a.h.p.与去极化过程中前几个动作电位的频率增加有关。这与阻断慢速a.h.p所导致的动作电位的大量增加是截然不同的。结果支持了一个结论，即快速a.h.p.是由TEA和电压敏感的Ca2+激活的K+电流IC产生的。该电流参与尖峰复极化，并在返回静息电位时关闭。因此，阻塞IC对由单独的膜电流引起的缓慢a.h.p.没有影响。
1. Intracellular recording from hippocampal CA1 pyramidal cells in the slice preparation was used to analyse the pharmacological sensitivity of action potential repolarization and the hyperpolarization that follow the action potential. The Ca2+-activated after-hyperpolarizations (a.h.p.s.) could be divided into a fast a.h.p. with a time course of milliseconds, and a slow a.h.p. which lasted for a few seconds at a temperature of 30.degree. C. 2. The repolarization of the action potential is sensitive to the Ca2+ channel blocker Cd2+. This effect is simultaneous with a block of the fast a.h.p. which follows immediately upon the repolarization of the action potential. The slow a.h.p. was also blocked by Cd2+. 3. Low concentrations of the K+ channel blocker, tetraethylammonium (TEA: 200-500 .mu.M), block the fast a.h.p. and slow down action potential repolarization. The slow a.h.p. was not affected by low concentrations of TEA. 4. The action potential repolarization and the fast a.h.p. are also reversibly sensitive to charybdotoxin. This agent had no effect on the slow a.h.p. 5. When EGTA or BAPTA were added to the normal recording electrolyte (KMeSO4), the generation of slow a.h.p.s. was prevented. In addition, cells impaled with BAPTA-containing electrodes displayed broader action potentials and much reduced fast a.h.p.s compared to recordings made with electrodes containing KMeSO3 alone or with EGTA. 6. The slow a.h.p. can be eliminated by noradrenaline, 8-bromocyclic AMP or carbachol. Under these conditions there are no effects on the fast a.h.p. or on action potential duration. 7. Block of the fast a.h.p. with TEA or CTX (charybdotoxin) is associated with an increased frequency of the first few action potentials during a depolarization. This is a quite distinct effect from the greatly increased number of action potentials which results from block of the slow a.h.p. 8. The results support a conclusion that the fast a.h.p. is generated by the TEA- and voltage-sensitive Ca2+-activated K+ current, IC. This current is involved in spike repolarization and turns off upon the return to resting potential. Thus block of IC has no effect on the slow a.h.p. which is caused by a separate membrane current.