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铯诱导大鼠视上核神经元去极化的离子基础。

Ionic basis of the caesium-induced depolarisation in rat supraoptic nucleus neurones.

作者信息

Ghamari-Langroudi M, Bourque C W

机构信息

Centre for Research in Neuroscience, Montreal General Hospital and McGill University, 1650 Cedar Avenue, Montreal, QC, Canada H3G 1A4.

出版信息

J Physiol. 2001 Nov 1;536(Pt 3):797-808. doi: 10.1111/j.1469-7793.2001.00797.x.

Abstract
  1. The effects of external Cs(+) on magnocellular neurosecretory cells were studied during intracellular recordings from 93 supraoptic nucleus neurones in superfused explants of rat hypothalamus. 2. Bath application of 3-5 mM Cs(+) provoked reversible membrane depolarisation and increased firing rate in all of the neurones tested. Voltage-current analysis revealed an increase in membrane resistance between -120 and -55 mV. The increase in resistance was greater below -85 mV than at more positive potentials. 3. Voltage-clamp analysis showed that external Cs(+) blocked the hyperpolarisation-activated inward current, I(H). Under current clamp, application of ZD 7288, a selective blocker of I(H), caused an increase in membrane resistance at voltages < or = -65 mV. Voltage-current analysis further revealed that blockade of I(H) caused hyperpolarisation when the initial voltage was < -60 mV but had no effect at more positive values. 4. Current- and voltage-clamp analysis of the effects of Cs(+) in the presence of ZD 7288, or ZD 7288 and tetraethyl ammonium (TEA), revealed an increase in membrane resistance throughout the range of voltages tested (-120 to -45 mV). The current blocked by Cs(+) in the absence of I(H) was essentially voltage independent and reversed at -100 mV. The reversal potential shifted by +22.7 mV when external [K(+)] was increased from 3 to 9 mM. We conclude that, in addition to blocking I(H), external Cs(+) blocks a leakage K(+) current that contributes significantly to the resting potential of rat magnocellular neurosecretory cells.
摘要
  1. 在对大鼠下丘脑灌流外植体中93个视上核神经元进行细胞内记录期间,研究了细胞外Cs(+)对大细胞神经分泌细胞的影响。2. 向浴槽中加入3 - 5 mM Cs(+)可引起所有受试神经元出现可逆性膜去极化并增加放电频率。电压 - 电流分析显示,在 - 120至 - 55 mV之间膜电阻增加。在 - 85 mV以下电阻增加幅度大于更正电位时。3. 电压钳分析表明,细胞外Cs(+)阻断了超极化激活内向电流I(H)。在电流钳记录下,应用I(H)的选择性阻断剂ZD 7288,在电压≤ - 65 mV时可引起膜电阻增加。电压 - 电流分析进一步显示,阻断I(H)在初始电压< - 60 mV时引起超极化,但在更正电位时无作用。4. 在存在ZD 7288或ZD 7288与四乙铵(TEA)的情况下,对Cs(+)作用进行电流钳和电压钳分析,发现在整个测试电压范围(- 120至 - 45 mV)内膜电阻均增加。在不存在I(H)时被Cs(+)阻断的电流基本与电压无关,且在 - 100 mV时反转。当细胞外[K(+)]从3 mM增加到9 mM时,反转电位偏移 + 22.7 mV。我们得出结论,除了阻断I(H)外,细胞外Cs(+)还阻断了一种对大鼠大细胞神经分泌细胞静息电位有显著贡献的外向K(+)电流。

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