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热敏钾通道 TREK-1 有助于 Grueneberg 神经节神经元对冷觉刺激的反应。

The thermosensitive potassium channel TREK-1 contributes to coolness-evoked responses of Grueneberg ganglion neurons.

机构信息

Institute of Physiology, University of Hohenheim, Garbenstr. 30, 70599, Stuttgart, Germany.

出版信息

Cell Mol Neurobiol. 2014 Jan;34(1):113-22. doi: 10.1007/s10571-013-9992-x. Epub 2013 Oct 8.

DOI:10.1007/s10571-013-9992-x
PMID:24101433
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11488964/
Abstract

Neurons of the Grueneberg ganglion (GG) residing in the vestibule of the murine nose are activated by cool ambient temperatures. Activation of thermosensory neurons is usually mediated by thermosensitive ion channels of the transient receptor potential (TRP) family. However, there is no evidence for the expression of thermo-TRPs in the GG, suggesting that GG neurons utilize distinct mechanisms for their responsiveness to cool temperatures. In search for proteins that render GG neurons responsive to coolness, we have investigated whether TREK/TRAAK channels may play a role; in heterologous expression systems, these potassium channels have been previously found to close upon exposure to coolness, leading to a membrane depolarization. The results of the present study indicate that the thermosensitive potassium channel TREK-1 is expressed in those GG neurons that are responsive to cool temperatures. Studies analyzing TREK-deficient mice revealed that coolness-evoked responses of GG neurons were clearly attenuated in these animals compared with wild-type conspecifics. These data suggest that TREK-1 channels significantly contribute to the responsiveness of GG neurons to cool temperatures, further supporting the concept that TREK channels serve as thermoreceptors in sensory cells. Moreover, the present findings provide the first evidence of how thermosensory GG neurons are activated by given temperature stimuli in the absence of thermo-TRPs.

摘要

位于鼠鼻前庭的 Grueneberg 神经节(GG)神经元可被环境低温激活。热敏神经元的激活通常由瞬时受体电位(TRP)家族的热敏离子通道介导。然而,目前尚无证据表明 GG 中存在热 TRP 的表达,这表明 GG 神经元对低温的反应可能采用了不同的机制。为了寻找使 GG 神经元对冷刺激敏感的蛋白,我们研究了 TREK/TRAAK 通道是否可能发挥作用;在异源表达系统中,先前发现这些钾通道在暴露于低温时会关闭,导致膜去极化。本研究结果表明,对冷刺激敏感的钾通道 TREK-1 在那些对低温敏感的 GG 神经元中表达。分析 TREK 缺失小鼠的研究表明,与野生型同窝小鼠相比,这些动物 GG 神经元对冷刺激的反应明显减弱。这些数据表明,TREK-1 通道对 GG 神经元对低温的反应有重要贡献,进一步支持了 TREK 通道作为感觉细胞热敏感受器的概念。此外,本研究结果首次提供了在没有热 TRP 的情况下,特定温度刺激如何激活热敏 GG 神经元的证据。

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本文引用的文献

1
Chemo- and thermosensory responsiveness of Grueneberg ganglion neurons relies on cyclic guanosine monophosphate signaling elements.格鲁内贝格神经节神经元的化学和热感觉反应性依赖于环磷酸鸟苷信号元件。
Neurosignals. 2011;19(4):198-209. doi: 10.1159/000329333. Epub 2011 Aug 31.
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Grueneberg ganglion neurons are activated by a defined set of odorants.格鲁恩伯格神经节神经元被一组特定的气味激活。
Chem Senses. 2011 Mar;36(3):271-82. doi: 10.1093/chemse/bjq124. Epub 2010 Dec 9.
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Dominant negative effects of a non-conducting TREK1 splice variant expressed in brain.在脑中表达的不传导 TREK1 剪接变异体的显性负效应。
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Grueneberg ganglion neurons are finely tuned cold sensors.格吕内伯格神经节神经元是精细调节的冷感受器。
J Neurosci. 2010 Jun 2;30(22):7563-8. doi: 10.1523/JNEUROSCI.0608-10.2010.
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The Grueneberg ganglion: a novel sensory system in the nose.格林伯格神经节:鼻腔内的新型感觉系统。
Histol Histopathol. 2010 Jul;25(7):909-15. doi: 10.14670/HH-25.909.
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The cyclic nucleotide-gated ion channel CNGA3 contributes to coolness-induced responses of Grueneberg ganglion neurons.环核苷酸门控离子通道 CNGA3 有助于 Grueneberg 神经节神经元对冷刺激的反应。
Cell Mol Life Sci. 2010 Jun;67(11):1859-69. doi: 10.1007/s00018-010-0296-8. Epub 2010 Feb 18.
7
Immunohistochemical colocalization of TREK-1, TREK-2 and TRAAK with TRP channels in the trigeminal ganglion cells.三叉神经节细胞中 TREK-1、TREK-2 和 TRAAK 与瞬时受体电位(TRP)通道的免疫组织化学共定位
Neurosci Lett. 2009 Apr 24;454(2):129-33. doi: 10.1016/j.neulet.2009.02.069. Epub 2009 Mar 5.
8
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EMBO J. 2009 May 6;28(9):1308-18. doi: 10.1038/emboj.2009.57. Epub 2009 Mar 12.
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Glucose inhibition persists in hypothalamic neurons lacking tandem-pore K+ channels.缺乏串联孔钾通道的下丘脑神经元中存在葡萄糖抑制现象。
J Neurosci. 2009 Feb 25;29(8):2528-33. doi: 10.1523/JNEUROSCI.5764-08.2009.
10
Grueneberg ganglion neurons respond to cool ambient temperatures.格鲁内贝格神经节神经元对凉爽的环境温度有反应。
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