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哇巴因增强家兔内脏初级传入神经元中钙依赖性钾离子电导。

Ouabain augments calcium-dependent potassium conductance in visceral primary afferent neurones of the rabbit.

作者信息

Higashi H, Katayama Y, Morita K, North R A

机构信息

Department of Autonomic Physiology, Tokyo Medical and Dental University, Japan.

出版信息

J Physiol. 1987 Aug;389:629-45. doi: 10.1113/jphysiol.1987.sp016675.

Abstract
  1. The effects of ouabain (1 nM-100 microM) on the membrane properties of rabbit visceral primary afferent neurones (nodose ganglion cells) were studied with intracellular recordings and voltage-clamp techniques in vitro. 2. Ouabain (greater than or equal to 1 microM) often produced a membrane hyperpolarization associated with a fall of membrane resistance in type C neurones. The ouabain-induced hyperpolarization reversed in polarity at about -90 mV. These suggest that the ouabain-induced hyperpolarization is due to an increase in potassium conductance. 3. Both the peak amplitude and the duration of the after-hyperpolarization following an action potential were reversibly increased with increasing concentration of ouabain. In tetraethylammonium (TEA, 10-20 mM) and tetrodotoxin (TTX, 1-10 microM), the duration of both the calcium-dependent action potential and the after-hyperpolarization following the action potential was prolonged by ouabain (greater than or equal to 10 nM). 4. A depolarizing command pulse evoked a slow outward current in TEA (10-20 mM) and TTX (1-10 microM). This was increased in amplitude and prolonged in duration by ouabain (100 nM-1 microM). Such augmentation of the slow outward current by ouabain was usually associated with an increase in a slow inward current during the period of the depolarizing command pulse. 5. An outward current produced by the calcium ionophore A23187 was reversibly augmented by ouabain (greater than or equal to 10 nM). 6. An outward current caused by exchanging a potassium-free superfusion solution for one containing 4.7 or 10 mM-potassium was completely abolished by ouabain (greater than or equal to 10 nM). 7. The hyperpolarization elicited by intracellular injection of calcium was reversibly prolonged by either ouabain (1 microM) or caffeine (10 nM). 8. These results suggest that ouabain augments the after-hyperpolarization both by an increase in calcium influx across the cellular membrane and by an increase in intracellular calcium concentration.
摘要
  1. 采用细胞内记录和电压钳技术,在体外研究了哇巴因(1纳摩尔至100微摩尔)对兔内脏初级传入神经元(结状神经节细胞)膜特性的影响。2. 哇巴因(大于或等于1微摩尔)常使C型神经元产生膜超极化,并伴有膜电阻下降。哇巴因诱导的超极化在约 -90毫伏时极性反转。这些表明哇巴因诱导的超极化是由于钾电导增加。3. 随着哇巴因浓度增加,动作电位后的超极化峰值幅度和持续时间均可逆性增加。在四乙铵(TEA,10 - 20毫摩尔)和河豚毒素(TTX,1 - 10微摩尔)存在时,哇巴因(大于或等于10纳摩尔)可延长钙依赖性动作电位及动作电位后的超极化持续时间。4. 去极化指令脉冲在TEA(10 - 20毫摩尔)和TTX(1 - 10微摩尔)中诱发缓慢外向电流。哇巴因(100纳摩尔至1微摩尔)可增加该电流幅度并延长其持续时间。哇巴因对缓慢外向电流的这种增强通常与去极化指令脉冲期间缓慢内向电流增加有关。5. 钙离子载体A23187产生的外向电流可被哇巴因(大于或等于10纳摩尔)可逆性增强。6. 用含4.7或10毫摩尔钾的溶液替换无钾灌流液所引起的外向电流,可被哇巴因(大于或等于10纳摩尔)完全消除。7. 细胞内注射钙所引发的超极化可被哇巴因(1微摩尔)或咖啡因(10纳摩尔)可逆性延长。8. 这些结果表明,哇巴因通过增加跨细胞膜的钙内流和增加细胞内钙浓度来增强动作电位后的超极化。

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