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成年大鼠心内神经元中的钾电流

Potassium currents in adult rat intracardiac neurones.

作者信息

Xi-Moy S X, Dun N J

机构信息

Department of Anatomy and Neurobiology, Medical College of Ohio, Toledo 43614, USA.

出版信息

J Physiol. 1995 Jul 1;486 ( Pt 1)(Pt 1):15-31. doi: 10.1113/jphysiol.1995.sp020787.

Abstract
  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)
摘要
  1. 运用单电极电压钳技术,对成年大鼠离体心脏副交感神经神经元的钾离子电流特性进行了研究。2. 当细胞膜钳制在接近静息电位(-60mV)时,可观察到一种超极化激活的内向整流电流。在-150mV时,缓慢发展的内向松弛电流平均幅值为450pA,激活阈值为-60至-70mV,在-120mV时松弛时间常数为41ms。该电流可被1mM的铯离子(Cs+)可逆性阻断,且随着细胞外钾离子([K+]o)和钠离子([Na+]o)浓度降低而减小,表明这种内向整流电流可能是一种时间和电压依赖性的钠钾电流。3. 从-80mV的钳制电位进行阶跃去极化,可诱发一个短暂的(在-40mV时<100ms)外向钾离子电流(IA),该电流可被1mM的4-氨基吡啶(4-AP)阻断。IA失活的时间常数在-50mV时为20ms,在-20mV时为16ms。稳态激活和失活(去除)曲线在-70至-40mV之间有小范围重叠;IA的反转电位接近钾离子平衡电位(EK)。4. 从去极化电位(即-30mV)进行阶跃超极化,可揭示与一种时间和电压依赖性电流失活相关的缓慢内向松弛。在超极化程度更高的电位下,内向松弛变得更快,在4.7mM和15mM的[K+]o中,分别在-85mV和-53mV时发生反转。该电流可被20μM的毒蕈碱和1mM的钡离子(Ba2+)阻断,但不受1mM的Cs+影响;这种电流可能对应于M电流(IM)。5. 在存在3μM河豚毒素(TTX)、1mM 4-AP和1mM Ba2+的情况下,将细胞膜钳制在接近静息电位,可诱发去极化激活的外向钾离子电流。随着[K+]o升高,外向松弛和尾电流的幅值变小。在无钙溶液中,外向尾电流减小,加入10mM四乙铵(TEA)后残余电流消失;反转电位的移动方向符合能斯特方程预测。这些发现提示存在延迟整流钾离子电流和钙激活钾离子电流。6. 用TEA、Ba2+和4-AP灌注,但不用Cs+灌注,可在一些原本静止的心脏内神经元中诱发节律性放电。(摘要截断于400字)
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2825/1156493/88b76e79f7b0/jphysiol00315-0020-a.jpg

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