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10
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J Physiol. 1974 Oct;242(2):321-51. doi: 10.1113/jphysiol.1974.sp010710.

本文引用的文献

1
Some properties of the external activation site of the sodium pump in crab nerve.蟹神经中钠泵外部激活位点的一些特性
J Physiol. 1966 Jul;185(2):270-97. doi: 10.1113/jphysiol.1966.sp007987.
2
On the permeability of mammalian non-myelinated fibres to sodium and to lithium ions.关于哺乳动物无髓鞘纤维对钠离子和锂离子的通透性
J Physiol. 1963 Jan;165(1):130-40. doi: 10.1113/jphysiol.1963.sp007047.
3
Depolarization of the motor end-plate by decamethonium and acetylcholine.十烃季铵和乙酰胆碱对运动终板的去极化作用。
J Physiol. 1951 Sep;115(1):41-73. doi: 10.1113/jphysiol.1951.sp004652.
4
Contractures and permeability changes produced by acetylcholine in depolarized denervated muscle.乙酰胆碱在去神经支配的去极化肌肉中产生的挛缩和通透性变化。
J Physiol. 1961 Nov;159(1):111-27. doi: 10.1113/jphysiol.1961.sp006796.
5
The permeability of frog muscle fibres to lithium ions.蛙肌纤维对锂离子的通透性。
J Physiol. 1959 Oct;147(3):626-38. doi: 10.1113/jphysiol.1959.sp006265.
6
Active transport of cations in giant axons from Sepia and Loligo.乌贼和枪乌贼巨大轴突中阳离子的主动运输。
J Physiol. 1955 Apr 28;128(1):28-60. doi: 10.1113/jphysiol.1955.sp005290.
7
ENZYMATIC BASIS FOR ACTIVE TRANSPORT OF NA+ AND K+ ACROSS CELL MEMBRANE.钠离子和钾离子跨细胞膜主动运输的酶学基础
Physiol Rev. 1965 Jul;45:596-617. doi: 10.1152/physrev.1965.45.3.596.
8
AN ELECTROGENIC SODIUM PUMP IN SNAIL NERVE CELLS.蜗牛神经细胞中的一种生电钠泵。
Comp Biochem Physiol. 1965 Jan;14:167-83. doi: 10.1016/0010-406x(65)90017-4.
9
A COMPARISON OF THE GANGLION POTENTIALS AND BLOCK PRODUCED BY ACETYLCHOLINE AND TETRAMETHYLAMMONIUM.乙酰胆碱和四甲铵产生的神经节电位及阻断作用的比较
Br J Pharmacol Chemother. 1964 Aug;23(1):80-9. doi: 10.1111/j.1476-5381.1964.tb01568.x.
10
GANGLIONIC BLOCKADE PRODUCED IN SYMPATHETIC GANGLIA BY CHOLINOMIMETIC DRUGS.拟胆碱药在交感神经节中产生的神经节阻断作用。
J Pharmacol Exp Ther. 1963 Sep;141:333-42.

从大鼠离体颈上神经节去除去极化剂后超极化的起源。

Origin of the after-hyperpolarization that follows removal of depolarizing agents from the isolated superior cervical ganglion of the rat.

作者信息

Brown D A, Brownstein M J, Scholfield C N

出版信息

Br J Pharmacol. 1972 Apr;44(4):651-71. doi: 10.1111/j.1476-5381.1972.tb07305.x.

DOI:10.1111/j.1476-5381.1972.tb07305.x
PMID:4625268
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1665991/
Abstract
  1. Potential changes in isolated rat superior cervical ganglia following addition and removal of depolarizing agents were recorded using a moving-fluid extracellular electrode system.2. Ganglionic negativity produced by carbachol was followed by a pronounced ganglionic positivity on washing. This after-positivity was attributed to hyperpolarization of the ganglion cells since it was unaffected by crushing the postganglionic trunk.3. The after-hyperpolarization was selectively depressed by (a) cooling (Q(10) 2.3), (b) metabolic inhibitors (cyanide, azide, 2,4-dinitrophenol), (c) reducing K(+) or substituting Cs(+) for K(+), (d) ouabain, and (e) substituting Li(+) for Na(+). This suggested a close dependence on active Na(+) transport.4. When K(+) was restored to K(+)-free solution, or the preparation was warmed rapidly, or when metabolic inhibitors were washed away, the hyperpolarization was rapidly regenerated. The effect of restoring K(+) indicated that the hyperpolarization was generated directly by the Na(+) pump.5. The hyperpolarization was not altered by replacing Cl(-) with isethionate, indicating that the voltage change produced by the Na(+) current was not modified by passive Cl(-) movements.6. Hexamethonium added to the washout fluid augmented the after-hyperpolarization, suggesting that there was a high (cationic) leak current due to continued receptor-activation on washing with normal Krebs solution.7. The hyperpolarization was reduced by omission of Ca(2+) and restored by addition of Mg(2+). This was considered to result from changes in passive membrane permeability.8. The time-course of post-carbachol hyperpolarization accorded with a Na(+) extrusion process whose rate was directly proportional to Na(+) with a rate constant of 0.38+/-0.02 min(-1) at 23-27 degrees C.9. With increasing concentrations of carbachol, the amplitude of the hyperpolarization increased in proportion to the preceding depolarization, but the rate constant of the hyperpolarization was unchanged.
摘要

  1. 使用流动液体细胞外电极系统记录了离体大鼠颈上神经节在添加和去除去极化剂后可能发生的变化。

  2. 卡巴胆碱引起的神经节负电位之后，冲洗时会出现明显的神经节正电位。这种后正电位归因于神经节细胞的超极化，因为它不受节后干挤压的影响。

  3. 后超极化被以下因素选择性抑制：(a) 冷却（Q(10) 2.3），(b) 代谢抑制剂（氰化物、叠氮化物、2,4-二硝基苯酚），(c) 降低K(+) 或用Cs(+) 替代K(+)，(d) 哇巴因，以及(e) 用Li(+) 替代Na(+)。这表明其与主动Na(+) 转运密切相关。

  4. 当将K(+) 恢复到无K(+) 溶液中，或制剂快速升温，或代谢抑制剂被冲洗掉时，超极化会迅速再生。恢复K(+) 的效果表明超极化是由Na(+) 泵直接产生的。

  5. 用羟乙磺酸盐替代Cl(-) 时，超极化没有改变，这表明由Na(+) 电流产生的电压变化不受被动Cl(-) 移动的影响。

  6. 添加到冲洗液中的六甲铵增强了后超极化，这表明在用正常 Krebs 溶液冲洗时，由于受体持续激活，存在高（阳离子）漏电流。

  7. 去除Ca(2+) 会降低超极化，添加Mg(2+) 则可使其恢复。这被认为是由被动膜通透性的变化导致的。

  8. 卡巴胆碱后超极化的时间进程符合Na(+) 排出过程，其速率与Na(+) 成正比，在23 - 27摄氏度时速率常数为0.38 +/- 0.02 min(-1)。

  9. 随着卡巴胆碱浓度的增加，超极化的幅度与先前的去极化成比例增加，但超极化的速率常数不变。