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A comparison of sodium currents in rat and frog myelinated nerve: normal and modified sodium inactivation.

机译:大鼠和青蛙有髓神经钠电流的比较:正常和改良的钠失活。

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摘要

1. Sodium currents were measured under voltage-clamp conditions in Ranvier nodes of rat and frog nerve fibres at 20 degrees C. Voltage errors due to the resistance in series with the nodal membrane were minimized by reducing sodium currents with tetrodotoxin in the extracellular solutions. 2. The stationary and kinetic properties of sodium activation and inactivation were determined for a wide range of potentials (V) from -40 to 160 mV with respect to the initial holding level (V = 0 mV). 3. The curves m infinity(V) and h infinity(V) of stationary sodium activation and inactivation were not different in rat and frog fibres. 4. The time constants tau m, tau h of sodium activation and inactivation were normally larger in the rat than in the frog. At moderate depolarizations (0 less than or equal to V less than or equal to 80 mV) tau m in the rat was 15-50% larger; the ratio of the rat to the frog tau h values was usually smaller. Thus tau m/tau h = 0.116 for the rat and 0.0965 for the frog at V = 60 mV (potential with maximum peak sodium inward current). 5. Sodium inactivation in rat nerve was slowed and became incomplete by application of intra-axonal iodate or by treatment with external Anemonia toxin II (ATX II), chloramine-T or Ruthenium Red. Peak sodium currents were not increased by these substances. 6. Wash-out of ATX II from frog nerve was rapid and complete but partly irreversible in rat nerve. This suggests different properties or accessibilities of sodium channels in frog and rat nodes.
机译:1.在电压钳制条件下,于20摄氏度在大鼠和青蛙神经纤维的Ranvier节点中测量钠电流。通过降低细胞外溶液中的河豚毒素的钠电流,可将因与结膜串联的电阻引起的电压误差降至最低。 2.在相对于初始保持水平(V = 0 mV)的-40至160 mV的宽范围电势(V)中,确定了钠活化和失活的稳态和动力学性质。 3.在大鼠和青蛙纤维中,固定钠活化和失活的曲线m infinity(V)和h infinity(V)均无差异。 4.在大鼠中,时间常数taum,钠活化和失活的τau通常比青蛙大。在适度的去极化(0小于或等于V小于或等于80 mV)下,大鼠的tau m大15-50%;大鼠与青蛙的tau h值之比通常较小。因此,在V = 60 mV(具有最大钠内向电流峰值的电位)下,大鼠的tau m / tau h = 0.116,青蛙的0.0965。 5.通过应用轴突内碘酸盐或用外部Anemonia毒素II(ATX II),氯胺-T或钌红处理,可减缓大鼠神经中的钠失活,使其不完全。这些物质不会增加钠的峰值电流。 6.从蛙神经中快速清除ATX II,但在大鼠神经中部分不可逆。这表明青蛙和大鼠淋巴结中钠通道的性质或可及性不同。

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