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首页> 外文期刊>Neuron >TASK-1, a two-pore domain K+ channel, is modulated by multiple neurotransmitters in motoneurons.
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TASK-1, a two-pore domain K+ channel, is modulated by multiple neurotransmitters in motoneurons.

机译：TASK-1是一个两孔域K +通道，由运动神经元中的多种神经递质调节。

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摘要

Inhibition of "leak" potassium (K+) channels is a widespread CNS mechanism by which transmitters induce slow excitation. We show that TASK-1, a two pore domain K+ channel, provides a prominent leak K+ current and target for neurotransmitter modulation in hypoglossal motoneurons (HMs). TASK-1 mRNA is present at high levels in motoneurons, including HMs, which express a K+ current with pH- and voltage-dependent properties virtually identical to those of the cloned channel. This pH-sensitive K+ channel was fully inhibited by serotonin, norepinephrine, substance P, thyrotropin-releasing hormone, and 3,5-dihydroxyphenylglycine, a group I metabotropic glutamate receptor agonist. The neurotransmitter effect was entirely reconstituted in HEK 293 cells coexpressing TASK-1 and the TRH-R1 receptor. Given its expression patterns and the widespread prevalence of this neuromodulatory mechanism, TASK-1 also likely supports this action in other CNS neurons.
机译：抑制“泄漏”钾（K +）通道是一种广泛的中枢神经系统机制，通过该机制发射机可以诱导慢激发。我们显示，TASK-1，两个孔结构域K +通道，提供了一个突出的泄漏K +电流，并为舌下运动神经元（HMs）中的神经递质调节提供了目标。 TASK-1 mRNA在包括HMs在内的运动神经元中以高水平存在，它们表达的K +电流具有与克隆通道相同的pH和电压依赖性特性。该pH敏感的K +通道被5-羟色胺，去甲肾上腺素，P物质，促甲状腺激素释放激素和3,5-二羟基苯基甘氨酸（一种I型代谢型谷氨酸受体激动剂）完全抑制。神经递质的作用完全在共表达TASK-1和TRH-R1受体的HEK 293细胞中重建。鉴于其表达模式和这种神经调节机制的广泛流行，TASK-1也可能在其他CNS神经元中支持这种作用。

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