Potassium currents in adult rat intracardiac neurones.
Potassium currents in adult rat intracardiac neurones.
复制标题
成年大鼠心内神经元的钾电流。
DOI：
10.1113/jphysiol.1995.sp020787
复制
发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Dun,NJ
中科院分区：
文献类型：
--
作者：
Xi-Moy,SX;Dun,NJ
1.用单电极电压钳技术研究了分离的成年大鼠心内副交感神经元钾电流的特性。2.当膜钳制到接近静息水平(-60 mV)时，出现超极化激活的内向整流电流。缓慢发展的内向松弛在-150 mV时的平均幅度为450pA，激活阈值为-60~-70 mV，在-120 mV时的松弛时间常数为41ms。该电流被Cs+(1 MM)可逆地阻断，并随着[K+]o和[Na+]o的减少而变小，表明该内向整流电流可能是一种时间和电压依赖性的Na(+)-K+电流。3.保持电位为-80 mV的阶跃去极化可诱发一种瞬时(-lt；100ms，-40 mV)外向钾电流(IA)，该电流可被4-氨基吡啶(4-AP，1 mM)阻断。IA失活时间常数在-50 mV时为20ms，在-20 mV时为16ms。稳态激活和失活去除曲线在-70 mV和-40 mV之间有微小重叠；IA的反转电位接近EK。4.去极化电位的阶跃超极化，即-30 mV，显示了与时间和电压相关的电流失活相关的缓慢的向内弛豫。在4.7 mM和15 mM[K+]o下，内向松弛在-85 mV和-53 mV时反转。该电流可被20微米的毒扁豆碱和1 mM的Ba2+所阻断，但不受Cs+(1 MM)的影响，此电流可能对应于M电流(IM)。5.在河豚毒素(TTX，3微米)、4-AP(1 MM)和Ba2+(1 MM)存在下，使膜靠近静息电位，可诱发去极化激活的外向K+电流。[K+]o越高，外向驰豫幅度越小，尾流越小。在无钙溶液中，外向尾流减小，加入10 mM的四乙基铵(TEA，10 mM)可消除残余电流；反转电位按能斯特方程所预测的方向移动。提示存在延迟整流钾电流和钙激活钾电流。6.灌流TEA、Ba2+和4-AP，但不灌流Cs+，可在一些原本静止的心内神经元中诱导节律性放电。
1. Properties of K+ currents were studied in isolated adult rat parasympathetic intracardiac neurones with the use of single‐electrode voltage‐clamp techniques. 2. A hyperpolarization‐activated inward rectifier current was revealed when the membrane was clamped close to the resting level (‐60 mV). The slowly developing inward relaxation had a mean amplitude of 450 pA at ‐150 mV, an activation threshold of ‐60 to ‐70 mV and a relaxation time constant of 41 ms at ‐120 mV. The current was reversibly blocked by Cs+ (1 mM) and became smaller with reduced [K+]o and [Na+]o, indicating that this inward rectifier current probably is a time‐ and voltage‐dependent Na(+)‐K+ current. 3. Step depolarizations from the holding potential of ‐80 mV evoked a transient (< 100 ms at ‐40 mV) outward K+ current (IA) which was blocked by 4‐aminopyridine (4‐AP, 1 mM). The time constants for IA inactivation were 20 ms at ‐50 mV and 16 ms at ‐20 mV. The steady‐state activation and (removal of) inactivation curve showed a small overlap between ‐70 and ‐40 mV; the reversal potential of IA was close to EK. 4. Step hyperpolarizations from the depolarized potentials, i.e. ‐30 mV, revealed a slow inward relaxation associated with the deactivation of a time‐ and voltage‐dependent current. The inward relaxation became faster at more hyperpolarized potentials and reversed at ‐85 and ‐53 mV in 4.7 and 15 mM [K+]o. This current was blocked by muscarine (20 microM) and Ba2+ (1 mM) but not affected by Cs+ (1 mM); this current may correspond to the M‐current (IM). 5. Depolarization‐activated outward K+ currents were evoked by holding the membrane close to the resting potential in the presence of tetrodotoxin (TTX, 3 microM), 4‐AP (1 mM) and Ba2+ (1 mM). The amplitude of the outward relaxation and the tail current became smaller as the [K+]o was elevated. The outward tail current was reduced in a Ca(2+)‐free solution and the residual current was eliminated by the addition of tetraethylammonium (TEA, 10 mM); the reversal potential was shifted in a direction predicted by the Nernst equation. These findings suggest the presence of delayed rectifier K+ current and Ca(2+)‐activated K+ current. 6. Superfusion of TEA, Ba2+ and 4‐AP, but not Cs+, induced rhythmic discharges in some of the otherwise quiescent intracardiac neurones.(ABSTRACT TRUNCATED AT 400 WORDS)