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首页> 外文期刊>The European Journal of Neuroscience >Kv3 voltage-gated potassium channels regulate neurotransmitter release from mouse motor nerve terminals.
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Kv3 voltage-gated potassium channels regulate neurotransmitter release from mouse motor nerve terminals.

机译：Kv3电压门控钾离子通道调节小鼠运动神经末梢释放神经递质。

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Abstract Voltage-gated potassium (Kv) channels are critical to regulation of neurotransmitter release throughout the nervous system but the roles and identity of the subtypes involved remain unclear. Here we show that Kv3 channels regulate transmitter release at the mouse neuromuscular junction (NMJ). Light- and electron-microscopic immunohistochemistry revealed Kv3.3 and Kv3.4 subunits within all motor nerve terminals of muscles examined [transversus abdominus, lumbrical and flexor digitorum brevis (FDB)]. To determine the roles of these Kv3 subunits, intracellular recordings were made of end-plate potentials (EPPs) in FDB muscle fibres evoked by electrical stimulation of tibial nerve. Tetraethylammonium (TEA) applied at low concentrations (0.05-0.5 mm), which blocks only a few known potassium channels including Kv3 channels, did not affect muscle fibre resting potential but significantly increased the amplitude of all EPPs tested. Significantly, this effect of TEA was still observed in the presence of the large-conductance calcium-activated potassium channel blockers iberiotoxin (25-150 nm) and Penitrem A (100 nm), suggesting a selective action on Kv3 subunits. Consistent with this, 15-microm 4-aminopyridine, which blocks Kv3 but not large-conductance calcium-activated potassium channels, enhanced evoked EPP amplitude. Unexpectedly, blood-depressing substance-I, a toxin selective for Kv3.4 subunits, had no effect at 0.05-1 microm. The combined presynaptic localization of Kv3 subunits and pharmacological enhancement of EPP amplitude indicate that Kv3 channels regulate neurotransmitter release from presynaptic terminals at the NMJ.
机译：摘要电压门控钾（Kv）通道对于调节整个神经系统中神经递质的释放至关重要，但尚不清楚所涉及亚型的作用和身份。在这里，我们显示Kv3通道调节小鼠神经肌肉接头（NMJ）的递质释放。光镜和电镜免疫组化显示所检查的肌肉的所有运动神经末梢内有Kv3.3和Kv3.4亚基[横腹，屈肌和短指屈肌（FDB）]。为了确定这些Kv3亚基的作用，对胫骨神经电刺激诱发的FDB肌纤维中的终板电位（EPP）进行了细胞内记录。以低浓度（0.05-0.5 mm）施用的四乙铵（TEA）仅阻断包括Kv3通道在内的少数几个已知的钾通道，不会影响肌纤维的静息电位，但会显着增加所有测试EPP的振幅。值得注意的是，在存在大电导钙激活钾通道阻滞剂埃博毒素（25-150 nm）和Penitrem A（100 nm）的情况下，仍观察到TEA的这种作用，表明对Kv3亚基具有选择性。与此相符的是，15微米的4-氨基吡啶可阻断Kv3，但不能阻止大电导钙激活的钾离子通道，从而增强了诱发的EPP振幅。出乎意料的是，对Kv3.4亚基具有选择性的毒素血液抑制物质-I在0.05-1微米处无效。 Kv3亚基的突触前定位和EPP振幅的药理学增强作用相结合，表明Kv3通道调节了NMJ从突触前末端的神经递质释放。

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