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铯离子可激活大鼠培养脊髓神经元中的氯离子通道。

Caesium ions activate chloride channels in rat cultured spinal cord neurones.

作者信息

Hughes D, McBurney R N, Smith S M, Zorec R

机构信息

MRC Neuroendocrinology Unit, Newcastle General Hospital.

出版信息

J Physiol. 1987 Nov;392:231-51. doi: 10.1113/jphysiol.1987.sp016778.

Abstract
  1. Caesium ions (Cs+), applied extracellularly, caused a decrease in the input resistance of cultured spinal cord (s.c.) neurones and depolarized the neurones when they contained 140 mM-CsCl. 2. The reversal potential for Cs+-activated currents shifted 56 mV on average for a 10-fold reduction in the intracellular chloride ion (Cl-) activity, indicating that the Cs+-activated currents were specific to Cl-. 3. The activation of Cl- currents by Cs+ was not due to the depolarization-evoked release of neurotransmitter from presynaptic terminals. We therefore suggest that Cs+ were acting directly on the extracellular surface of the s.c. neurones to activate Cl- currents. 4. Cs+-activated currents showed desensitization in the presence of 140 mM-Cs+. 5. The log-log plot of the dose-response data could be fitted with a straight line with a slope of 1.7 +/- 0.4 (n = 6), indicating that at least 2 Cs+ were needed to activate a single Cl- channel. The KD of the Cs+-induced response was greater than 69 mM. 6. In outside-out patches Cs+ activated single Cl- channels. These channels were not activated by sodium or potassium ions. 7. The Cs+-activated channels displayed a total of five distinct conductance states which had mean conductances of 20, 30, 43, 66 and 92 pS. The 30 and 43 pS states were the most frequently occurring states. 8. The conductance states of the Cs+-activated channel have the same conductances as those reported for gamma-aminobutyric acid (GABA)- and glycine-activated channels in rat s.c. neurones. We therefore conclude that Cs+ activate the same type of Cl- channel as GABA and glycine through an unidentified receptor.
摘要
  1. 细胞外施加铯离子(Cs+)会导致培养的脊髓神经元输入电阻降低,当神经元内含有140 mM CsCl时会使其去极化。2. 细胞内氯离子(Cl-)活性降低10倍时,Cs+激活电流的反转电位平均偏移56 mV,表明Cs+激活电流对Cl-具有特异性。3. Cs+对Cl-电流的激活并非由于突触前终末去极化诱发的神经递质释放。因此我们认为Cs+直接作用于脊髓神经元的细胞外表面以激活Cl-电流。4. 在140 mM Cs+存在的情况下,Cs+激活电流表现出脱敏现象。5. 剂量反应数据的对数-对数图可以用斜率为1.7±0.4(n = 6)的直线拟合,表明至少需要2个Cs+才能激活单个Cl-通道。Cs+诱导反应的KD大于69 mM。6. 在外侧向外膜片中,Cs+激活单个Cl-通道。这些通道不会被钠离子或钾离子激活。7. Cs+激活的通道共有五种不同的电导状态,其平均电导分别为20、30、43、66和92 pS。30和43 pS状态是最常出现的状态。8. Cs+激活通道的电导状态与大鼠脊髓神经元中γ-氨基丁酸(GABA)和甘氨酸激活通道的电导状态相同。因此我们得出结论,Cs+通过一种未知受体激活与GABA和甘氨酸相同类型的Cl-通道。

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