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青蛙节间钾离子通道和钠离子通道的特性

Properties of potassium and sodium channels in frog internode.

作者信息

Grissmer S

出版信息

J Physiol. 1986 Dec;381:119-34. doi: 10.1113/jphysiol.1986.sp016317.

Abstract
  1. Voltage-clamp experiments were performed on single frog internodes after acute demyelination with lysolecithin. The action of lysolecithin was stopped by washing out the lysolecithin with normal Ringer solution containing bovine albumin when the first delayed current was observed. After washing, the temperature was lowered from 25 to 15 degrees C. These procedures greatly prolonged the survival of the demyelinated internode up to 1 h. 2. External tetraethylammonium chloride (TEA+, 110 mM) reduced the K+ current in the internode only to 11% of the control value. 110 mM-TEA+ increased the time constant tau n of K+ activation by a factor of two in the node and by a factor of four in the internode. 120 mM-CsCl at the cut ends of the fibre also reduced the delayed outward current recorded at 60 mV in the internode to 11% of the control value, hardly changing the time constant tau n. 3. After a depolarization, the K+ tail current decayed in two phases, suggesting that the K+ conductance of the internodal membrane may be composed of at least two components, a slow one (gKs) and a fast one (gKf). As in the node, the fast K+ conductance of the internode can be further decomposed into two components (gKf1 and gKf2) with different activation potential ranges. The fast phase of the tail current was blocked by external application of 1 mM-4-aminopyridine (4-AP). The slow phase was almost unaltered by 1 mM-4-AP. The extrapolated slow tail current was 33% of the total tail current in the internode and 15% at the node, i.e. the proportion of slow K+ channels is larger in the internode than in the node. 4. Tetrodotoxin (TTX)-sensitive transient inward currents could be measured in the demyelinated internode, provided the large K+ currents were blocked by internal Cs+. The time course, TTX sensitivity, reversal potential and steady-state inactivation of the transient early inward current indicate that this current is caused mainly by Na+ passing through Na+ channels. 5. The density of K+ and Na+ channels in the demyelinated internode is estimated from the size of the K+ and Na+ current, respectively, and the capacity of the demyelinated segment. The K+ channel density of the internode seems to be about 20 times smaller than in the node, whereas the Na+ channel density in the internode appears to be about 500 times smaller than in the node.
摘要
  1. 用溶血卵磷脂对单个青蛙节间进行急性脱髓鞘处理后,进行电压钳实验。当观察到第一个延迟电流时,用含牛血清白蛋白的正常林格溶液冲洗掉溶血卵磷脂,终止其作用。冲洗后,将温度从25℃降至15℃。这些操作极大地延长了脱髓鞘节间的存活时间,长达1小时。2. 外部氯化四乙铵(TEA +,110 mM)仅将节间的K +电流降低至对照值的11%。110 mM - TEA +使节中K +激活的时间常数τn增加了两倍,节间增加了四倍。纤维切断端处的120 mM CsCl也将节间在60 mV记录的延迟外向电流降低至对照值的11%,几乎不改变时间常数τn。3. 去极化后,K +尾电流呈两个阶段衰减,这表明节间膜的K +电导可能至少由两个成分组成,一个慢成分(gKs)和一个快成分(gKf)。与节中一样,节间的快K +电导可进一步分解为两个具有不同激活电位范围的成分(gKf1和gKf2)。尾电流的快相被外部施加的1 mM 4 - 氨基吡啶(4 - AP)阻断。慢相几乎不受1 mM 4 - AP影响。节间外推的慢尾电流占总尾电流的33%,节中为15%,即节间慢K +通道的比例比节中更大。4. 只要大的K +电流被内部Cs +阻断,在脱髓鞘节间就可以测量到对河豚毒素(TTX)敏感的瞬时内向电流。瞬时早期内向电流的时间进程、TTX敏感性、反转电位和稳态失活表明,该电流主要由通过Na +通道的Na +引起。5. 根据K +和Na +电流的大小以及脱髓鞘节段的电容,分别估计脱髓鞘节间中K +和Na +通道的密度。节间的K +通道密度似乎比节中约小20倍,而节间的Na +通道密度似乎比节中约小500倍。

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