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急性分离的大鼠苍白球神经元表现出四种类型的高电压激活钙电流。

Acutely isolated neurons of the rat globus pallidus exhibit four types of high-voltage-activated Ca2+ current.

作者信息

Surmeier D J, Seno N, Kitai S T

机构信息

Department of Anatomy and Neurobiology, College of Medicine, University of Tennessee, Memphis 38163.

出版信息

J Neurophysiol. 1994 Mar;71(3):1272-80. doi: 10.1152/jn.1994.71.3.1272.

Abstract
  1. Large, projection-like neurons from the adult (> 3 wk post-natal) rat globus pallidus (GP) were acutely isolated and subjected to whole-cell voltage-clamp (n = 37). Ca2+ currents were isolated pharmacologically in cells with whole-cell capacitances of 15-34 pF. 2. With 5 mM Ba2+ as a charge carrier, whole-cell currents began to activate near -40 mV and peaked near 0 mV. Based on activation threshold and inactivation kinetics, currents appeared to be of the high-voltage-activated type. 3. Cd2+ blocked whole-cell currents with an IC50 near 2 microM. Currents activated at negative potentials were not relatively resistant to Cd2+, supporting the inference that low-voltage-activated currents were not prominent in these neurons. 4. The dihydropyridine, L-channel antagonist, nifedipine (5 microM), reduced peak current by 21 +/- 4% (SD) (n = 10). The dihydropyridine agonist, BayK 8644 (1-2 microM) enhanced peak current and slowed current deactivation (n = 4). 5. The N-channel antagonist, omega-conotoxin GVIA (omega-CgTx, 2 microM) blocked 25 +/- 7% of the peak whole-cell current (n = 10). The blocks produced by omega-CgTx and nifedipine were additive, blocking an average of 46 +/- 8% of the current (n = 10). 6. The current resistant to the selective N- and L-channel antagonists was partially blocked by the P-channel antagonist omega-agatoxin IVA (omega-AgTx, 100 nM). omega-AgTx blocked about one-half of the current not attributable to N- and L-type channels (22 +/- 5% of the total current, n = 5).(ABSTRACT TRUNCATED AT 250 WORDS)
摘要
  1. 从成年(出生后3周以上)大鼠苍白球(GP)中急性分离出大型、类似投射的神经元,并对其进行全细胞电压钳制(n = 37)。在全细胞电容为15 - 34 pF的细胞中,通过药理学方法分离出钙电流。2. 以5 mM Ba2+作为电荷载体,全细胞电流在接近 -40 mV时开始激活,在接近0 mV时达到峰值。基于激活阈值和失活动力学,电流似乎属于高电压激活型。3. Cd2+以接近2 microM的IC50阻断全细胞电流。在负电位激活的电流对Cd2+没有相对抗性,这支持了在这些神经元中低电压激活电流不显著的推断。4. 二氢吡啶类L通道拮抗剂硝苯地平(5 microM)使峰值电流降低了21 +/- 4%(标准差)(n = 10)。二氢吡啶类激动剂BayK 8644(1 - 2 microM)增强了峰值电流并减缓了电流失活(n = 4)。5. N通道拮抗剂ω-芋螺毒素GVIA(ω-CgTx,2 microM)阻断了25 +/- 7%的全细胞峰值电流(n = 10)。ω-CgTx和硝苯地平产生的阻断作用是相加的,平均阻断了46 +/- 8%的电流(n = 10)。6. 对选择性N和L通道拮抗剂有抗性的电流被P通道拮抗剂ω-蛛毒素IVA(ω-AgTx,100 nM)部分阻断。ω-AgTx阻断了约一半不归因于N型和L型通道的电流(占总电流的22 +/- 5%,n = 5)。(摘要截断于250字)

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