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蝾螈血小板激活后瞬态外向电流及其门控特性的变化。

Transient outward currents and changes of their gating properties after cell activation in thrombocytes of the newt.

作者信息

Kawa K

机构信息

Department of Pharmacology, Gunma University School of Medicine, Maebashi, Japan.

出版信息

J Physiol. 1987 Apr;385:189-205. doi: 10.1113/jphysiol.1987.sp016491.

DOI:10.1113/jphysiol.1987.sp016491
PMID:2443665
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1192344/
Abstract
  1. The electrical properties of the cell membrane of thrombocytes in the newt, Triturus pyrrhogaster, were studied using the whole-cell variation of the patch-electrode voltage-clamp technique. 2. In medium containing Ca2+ (1.8 mM), activated thrombocytes became round and then spread on the glass. Activation of thrombocytes was inhibited by the removal of external Ca2+ and addition of 1 w/v% albumin to the external media. 3. For thrombocytes kept in the resting state, depolarizations more positive than -30 mV evoked transient outward currents which decayed completely during the duration of the depolarization (150 ms). The half-decay time of the currents became smaller as the depolarizing pulse strengthened, reaching about 20 ms at +30 mV (20 degrees C). 4. The outward currents are identified as K+ currents, since (1) their reversal potential depended on extracellular K+ concentration and (2) the outward currents were suppressed either by external application of 4-aminopyridine (1 mM) or by internal application of Cs+ (120 mM). The monovalent cation selectivities of the K+ channels were evaluated from the reversal potential as Tl (1.68) greater than K(1.0) greater than Rb (0.89) greater than NH4 (0.13) greater than Na(less than 0.03). 5. When the thrombocytes had been activated, depolarization again evoked K+ currents. The currents, however, showed negligible or small decay during the duration of the depolarization (150 ms). The rate of recovery from preceding depolarization was also reduced to about one-sixth. 6. The sensitivity to 4-aminopyridine and the selectivity of the K+ channels were not changed by cell activation. 7. We conclude that during activation of thrombocytes the inactivation of the K+ channels is almost eliminated. Removal of inactivation of the K+ channels was also induced in resting thrombocytes by intracellular application of 4-bromoacetamide (50 microM).
摘要
  1. 采用膜片电极电压钳技术的全细胞模式,研究了蝾螈(Triturus pyrrhogaster)血小板细胞膜的电特性。2. 在含有Ca2+(1.8 mM)的培养基中,活化的血小板会变圆,然后铺展在玻璃上。去除细胞外Ca2+并向细胞外培养基中添加1 w/v%白蛋白可抑制血小板的活化。3. 对于处于静息状态的血小板,去极化超过 -30 mV会诱发瞬时外向电流,该电流在去极化持续期间(150 ms)完全衰减。随着去极化脉冲增强,电流的半衰减时间变小,在 +30 mV(20℃)时达到约20 ms。4. 外向电流被确定为K+电流,因为(1)其反转电位取决于细胞外K+浓度,并且(2)外向电流可被细胞外施加4-氨基吡啶(1 mM)或细胞内施加Cs+(120 mM)所抑制。根据反转电位评估K+通道的单价阳离子选择性为Tl(1.68)>K(1.0)>Rb(0.89)>NH4(0.13)>Na(<0.03)。5. 当血小板被激活后,去极化再次诱发K+电流。然而,在去极化持续期间(150 ms),这些电流显示出可忽略不计或很小的衰减。从前一次去极化恢复的速率也降低到约六分之一。6. 细胞活化不会改变对4-氨基吡啶的敏感性以及K+通道的选择性。7. 我们得出结论,在血小板活化过程中,K+通道的失活几乎被消除。在静息血小板中,通过细胞内施加4-溴乙酰胺(50 microM)也可诱导K+通道失活的消除。

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