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Characterization of 5-HT-sensitive potassium conductances in neonatal rat facial motoneurones in vitro

机译:新生大鼠面部运动神经元中5-HT敏感性钾电导的表征

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class="enumerated" style="list-style-type:decimal">The properties of the 5-HT-sensitive K+ conductance of neonatal rat facial motoneurones were examined in brainstem slices using whole-cell patch-clamp techniques.In a small proportion of motoneurones, 5-hydroxytryptamine (5-HT) evoked an inward current mediated solely by a decrease in K+ conductance. The reversal potential (V5-HT) was dependent on the external K+ concentration and the 5-HT-evoked current (I5-HT) displayed a linear current–voltage (I–V) relationship.In the remaining motoneurones, the 5-HT-evoked decrease in K+ conductance could only be observed in isolation once a concomitant 5-HT-mediated enhancement of the hyperpolarization-activated current, Ih, had been abolished with the Ih blocker, ZD-7288.External Cs+ also abolished the Ih-mediated component of I5-HT but, in addition, blocked part of the 5-HT-sensitive K+ current. At potentials hyperpolarized to V5-HT, Cs+ voltage dependently blocked I5-HT while at potentials depolarized to V5-HT, I5-HT was largely unaffected. Ba2+ and Rb+ had identical actions to Cs+ on the 5-HT-sensitive K+ current.The Ba2+-, Rb+- and Cs+-sensitive component of the 5-HT-sensitive K+ current inwardly rectified with a reversal potential that was dependent on the K+ equilibrium potential (EK).Replacing external Na+ with N-methyl-D-glucamine, blocking Ca2+ entry, or preventing an increase in intracellular [Ca2+] with BAPTA, all failed to alter I5-HT at potentials depolarized to EK.I5-HT at depolarized potentials was reversibly blocked by 4-aminopyridine (4 mm) but not tetraethylammonium chloride (30 mm) and did not show inactivation during depolarizing voltage pulses (1.5 s duration).The results suggest that, in addition to enhancing Ih, 5-HT modulates two distinct K+ conductances in neonatal rat facial motoneurones. The actions of Cs+, Ba2+ and Rb+ support the involvement of a member of the inwardly rectifying family of K+ channels while the other K+ channel may belong to the voltage-gated family.
机译:class =“ enumerated” style =“ list-style-type:decimal”> <!-list-behavior =枚举前缀-word = mark-type = decimal max-label-size = 0-> 使用全细胞膜片钳技术在脑干切片中检查了新生大鼠面部运动神经元对5-HT敏感的K + 电导的特性。 运动神经元5-羟色胺(5-HT)引起的内向电流仅由K + 电导的降低介导。反转电位(V5-HT)取决于外部K + 浓度,并且5-HT诱发电流(I5-HT)显示出线性的电流-电压(IV)关系。 / li> 在其余的运动神经元中,只有在5-HT介导的超极化激活电流伴随增强的情况下,才能单独观察到5-HT引起的K + 电导的降低,Ih已被Ih阻滞剂ZD-7288淘汰。 外部Cs + 也消除了Ih介导的I5-HT成分,但此外,它也阻止了部分I5-HT 5-HT敏感的K + 电流的变化。在超极化至V5-HT的电势下,Cs + 电压依赖性地阻断I5-HT,而在反极化至V5-HT的电势下,I5-HT基本上不受影响。 Ba 2 + 和Rb + 对5-HT敏感的K + 电流具有与Cs + 相同的作用 5-HT-的Ba 2 + -,Rb + -和Cs + 敏感成分敏感的K + 电流向内整流,其反向电位取决于K + 平衡电位(EK)。 替换外部Na + 用N-甲基-D-葡糖胺阻止Ca 2 + 进入,或防止BAPTA增加细胞内[Ca 2 + ]的增加,均失败改变去极化至EK的I5-HT。 I 5-去极化的I-HT被4-氨基吡啶(4 mm)可逆地阻断,但未被四乙基氯化铵(30 mm)阻断。 ),并且在去极化电压脉冲(持续1.5 s)期间未显示失活。 结果表明,除了增强 I h之外,5-HT还能调节两个不同的K <新生大鼠面部运动神经元中的sup> + 电导。 Cs + ,Ba 2 + 和Rb + 的作用支持K +的内向整流家族成员的参与通道,而另一个K + 通道可能属于电压门控家族。

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