The inactivating K+ current in GH3 pituitary cells and its modification by chemical reagents.
The inactivating K+ current in GH3 pituitary cells and its modification by chemical reagents.
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GH3垂体细胞失活K电流及其化学试剂修饰。
DOI：
10.1113/jphysiol.1989.sp017550
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Wagoner,PK
中科院分区：
文献类型：
--
作者：
Oxford,GS;Wagoner,PK
1. 应用全细胞和单通道记录技术研究了克隆性垂体细胞K+通道失活的通透性和门控性。2. 失活K+电流下通道的阳离子选择性顺序为Tl+ > K+ > Rb+ > NH4+。电导顺序（由电流幅值确定）为K+ = Tl+ > Rb+ > NH4+。3. 被4 -氨基吡啶（4 - AP）阻断的失活电流IK(i)在大于- 40 mV的正电压下激活，在该电压下一半失活。失活过程为两个指数的和，平均时间常数为21和82毫秒。失活遵循单指数时间过程。4. 从失活中恢复是缓慢的，电压依赖和多指数的，在细胞静息电位附近需要超过50秒。5. 随着外部K+浓度的增加，向外电流和斜率电导的大小增大。6. 细胞内和膜外贴片显示出具有门控和与全细胞电流相同药理特性的微电流。具有失活特性的单通道虽然很少观察到，但其平均斜率电导为6 - 8 pS。二硫二苯乙烯衍生物sit和蛋白质修饰试剂N -溴乙酰胺（NBA）在0.2 - 1 mM浓度下在细胞内应用数十分钟，显著减缓了K+电流的衰减（失活），并导致向外IK(i)的大小同时增加。8. 细胞外应用低浓度（1 - 100微米）和短时间（1 - 30秒）的NBA也减缓了失活。在低剂量下，这种效应在短期内是可逆的，但在长时间暴露后就不可逆了。9. 内外NBA均使稳态失活与电压的关系移动了+10 mV，并在大于0 mV的正电压下降低了失活。外源NBA的效力与‐80 ~ 0 mV的保持电位无关。在膜片外膜上施用NBA对细胞膜上的钾微电流和单通道没有影响。相反，NBA可逆地减缓了衰减，增加了小电流的大小，延长了从外部斑块记录的单个K+通道的打开时间。单通道电导未受NBA影响。（摘要删节为400字）
1. Whole‐cell and single‐channel recording techniques were applied to the study of the permeability and gating of inactivating K+ channels from clonal pituitary cells. 2. The cation selectivity sequence (measured from reversal potentials) for the channels underlying the inactivating K+ current was Tl+ greater than K+ greater than Rb+ greater than NH4+. The conductance sequence (determined from current amplitudes) was K+ = Tl+ greater than Rb+ greater than NH4+. 3. The inactivating current (IK(i] which was blocked by 4‐aminopyridine (4‐AP), activated at voltages more positive than ‐40 mV and half‐inactivated at that voltage. Inactivation proceeded as the sum of two exponentials with mean time constants of 21 and 82 ms. Deactivation followed a single‐exponential time course. 4. Recovery from inactivation was slow, voltage dependent and multi‐exponential, taking more than 50 s near the cell's resting potential. 5. The magnitudes of outward current and of slope conductance increased as the concentration of external K+ was increased. 6. On‐cell and outside‐out membrane patches revealed minicurrents with gating and pharmacological properties identical to whole‐cell currents. Single channels with inactivating characteristics, while rarely observed, had an average slope conductance of 6‐8 pS. 7. Intracellular application of the disulphonic stilbene derivative, SITS, and the protein‐modifying reagent, N‐bromoacetamide (NBA), at concentrations of 0.2‐1 mM for several tens of minutes dramatically slowed the decay (inactivation) of K+ currents and caused coincident increases in the magnitude of outward IK(i). 8. Extracellular application of NBA at much lower concentrations (1‐100 microM) and much shorter exposure times (1‐30 s) also slowed inactivation. This effect was reversible for brief applications at low doses, but became irreversible after longer exposures. 9. Both internal and external NBA shifted the steady‐state inactivation‐voltage relation by +10 mV and reduced inactivation at voltages more positive than 0 mV. 10. The efficacy of external NBA was independent of holding potential between ‐80 and 0 mV. 11. Potassium minicurrents and single channels recorded from on‐cell membrane patches were not affected by application of NBA to the extrapatch membrane. In contrast, NBA reversibly slowed the decay, increased the magnitude of minicurrents and prolonged the open times of single K+ channels recorded from outside‐out patches. The single‐channel conductance was unchanged by NBA.(ABSTRACT TRUNCATED AT 400 WORDS)
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作者：
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DOI：
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DOI：
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