首页> 美国卫生研究院文献>The Journal of Physiology >The slow calcium-dependent potassium current in a myenteric neurone of the guinea-pig ileum.
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The slow calcium-dependent potassium current in a myenteric neurone of the guinea-pig ileum.

机译:豚鼠回肠肌层神经元中钙依赖性钾电流缓慢。

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摘要

Experiments were performed in current-clamped and voltage-clamped after-hyperpolarizing (AH) neurones of the guinea-pig myenteric plexus to examine the properties of the potassium conductance (gK, Ca) underlying the slow calcium-activated after-hyperpolarization (VK, Ca). The action potential plateau lengthened by the addition of tetraethylammonium chloride (TEA) to the bathing medium was compared to VK, Ca. Results were consistent with enhanced calcium entry causing an increase of VK, Ca. 4-Aminopyridine (4-AP) directly reduced VK, Ca. Voltage-clamp data of gK, Ca were well fitted by a process with a delay (approximately equal to 60 ms) followed by exponential activation (time constant approximately equal to 300 ms) and inactivation (time constant approximately equal to 2 s). The presence of a small, much slower inactivating process was noted. Values for time constants were similar to those reported by Morita, North & Tokimasa (1982) and North & Tokimasa (1983) where gK, Ca was measured during VK, Ca subsequent to action potential stimulation. The relation between gK, Ca (or the calcium-activated potassium current IK, Ca) and estimated calcium influx resulting from short-duration calcium currents elicited at various voltages was compared. Both the integral of the calcium current and gK, Ca showed a similar dependence on the depolarizations used to elicit IK, Ca except there was a positive shift of about 4 mV for the gK, Ca curve. This shift was attributed to a requirement for calcium ions to prime the gK, Ca mechanism. An inward ion charge movement of about 8 pC was required before significant activation of gK, Ca occurred. After the 'priming' condition had been established, the sensitivity of gK, Ca to inward calcium current measured at the resting potential was about 500 pS/pC of inward charge. Large calcium entry obtained by prolonged calcium currents caused saturation of the peak amplitude of IK, Ca and initiated currents with slower time to peak amplitude and longer duration. Increasing the calcium concentration of the external solution provided proportionally larger IK, Ca currents before saturation. The saturation amplitude of IK, Ca (namely gK, Ca) was relatively unaffected.
机译:在豚鼠肌间神经丛的电流固定和电压固定的超极化后(AH)神经元中进行了实验,以检查慢钙激活的超极化后(VK, Ca)。将通过向浴液中添加四乙基氯化铵(TEA)延长的动作电位平台与VK,Ca进行比较。结果与钙进入增加导致VK,Ca增加一致。 4-氨基吡啶(4-AP)直接还原VK,Ca。 gK,Ca的电压钳位数据通过延迟(大约等于60 ms),指数激活(时间常数大约等于300 ms)和灭活(时间常数大约等于2 s)之后的过程很好地拟合。注意到存在一个小的,慢得多的灭活过程。时间常数的值类似于Morita,North和Tokimasa(1982)和North&Tokimasa(1983)报道的值,其中在动作电位刺激后的VK,Ca期间测量gK,Ca。比较了gK,Ca(或钙激活的钾电流IK,Ca)与在各种电压下引起的短期钙电流引起的估计钙流入之间的关系。钙电流的积分和gK,Ca都显示出与用于引起IK,Ca的去极化相似的依赖性,只是gK,Ca曲线有大约4 mV的正向偏移。这种转变归因于需要钙离子来启动gK,Ca机制。在显着激活gK,Ca之前,需要大约8 pC的向内离子电荷运动。建立“启动”条件后,在静止电位下测得的gK,Ca对内向钙电流的敏感性约为500 pS / pC。通过延长钙电流获得的大量钙进入会导致IK,Ca峰值幅度饱和,并且启动电流的峰值幅度会变慢,持续时间也会更长。增加外部溶液的钙浓度可按比例提供更大的IK,Ca饱和电流。 IK,Ca(即gK,Ca)的饱和幅度相对不受影响。

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