Mei Y A, Soriani O, Castel H, Vaudry H, Cazin L
Dept. of Physiology, Fudan University, Shanghai 200433, China.
Brain Res. 1998 May 18;793(1-2):271-8. doi: 10.1016/s0006-8993(98)00184-x.
The effects of adenosine on the voltage-sensitive delayed-rectifier K+ (IK) currents and hyperpolarization-activated cationic inward current (Ih) were studied in cultured frog melanotrophs using the whole-cell configuration of the patch-clamp technique. The A1 receptor agonist R-N6-phenylisopropyl-adenosine (R-PIA; 50 microM) reversibly increased IK. Perfusion of dibutyryl-cAMP (1 mM) in the external solution did not modify the R-PIA-induced enhancement of IK. Pretreatment of melanotrophs with pertussis toxin (1 microg/ml; 12 h) totally abolished the R-PIA-evoked response. Application of hyperpolarizing voltage pulses from -60 to -120 mV to melanotrophs induced a two-component inward current corresponding to an Ih-like conductance. This conductance was characterized by a high K+ selectivity and a low Na+ permeability and was resistant to tetrodotoxin (1 microM). R-PIA had no effect on Ih. The present study demonstrates that in frog melanotrophs adenosine inhibits the electrical activity by activating IK through an A1 receptor subtype coupled to a pertussis toxin-sensitive pathway independent of the cAMP/PKA system. This study also demonstrates the existence of a Ih conductance in frog melanotrophs which is not modulated by A1 receptors.
采用膜片钳技术的全细胞记录模式，在培养的青蛙黑素细胞中研究了腺苷对电压敏感性延迟整流钾电流（IK）和超极化激活阳离子内向电流（Ih）的影响。A1受体激动剂R-N6-苯基异丙基腺苷（R-PIA；50μM）可使IK可逆性增加。在细胞外溶液中灌注二丁酰环磷腺苷（1 mM）并不会改变R-PIA诱导的IK增强效应。用百日咳毒素（1μg/ml；12小时）预处理黑素细胞可完全消除R-PIA引起的反应。向黑素细胞施加从-60 mV至-120 mV的超极化电压脉冲可诱导出一种双成分内向电流，该电流对应于一种类似Ih的电导。这种电导的特征是具有高钾选择性和低钠通透性，并且对河豚毒素（1μM）具有抗性。R-PIA对Ih无影响。本研究表明，在青蛙黑素细胞中，腺苷通过与百日咳毒素敏感途径偶联的A1受体亚型激活IK，从而抑制电活动，该途径独立于环磷腺苷/蛋白激酶A系统。本研究还证明了青蛙黑素细胞中存在一种不受A1受体调节的Ih电导。
