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Serotonin type-1D receptor stimulation of A-type K+ channel decreases membrane excitability through the protein kinase A- and B-Raf-dependent p38 MAPK pathways in mouse trigeminal ganglion neurons
文献类型：期刊论文
| 作者 | Zhao, XY; Zhang, Y; Qin, WJ; Cao, JP; Zhang, Y; Ni, JQ; Sun, YG; Jiang, XH; Tao, J |
| 刊名 | CELLULAR SIGNALLING
 |
| 出版日期 | 2016 |
| 卷号 | 28期号:8页码:979-988 |
| 关键词 | DORSAL-ROOT GANGLION KV4.2 POTASSIUM CHANNEL BETA-GAMMA-SUBUNITS NEUROPATHIC PAIN SENSORY NEURONS ENHANCED EXCITABILITY INFLAMMATORY PAIN MELANOMA-CELLS ACTIVATION MODULATION |
| 通讯作者 | Tao, J (reprint author), Soochow Univ, Coll Med, Dept Physiol & Neurobiol, 199 Ren Ai Rd, Suzhou 215123, Peoples R China.,taoj@suda.edu.cn |
| 英文摘要 | Although recent studies have implicated serotonin 5-HT1B/D receptors in the nociceptive sensitivity of primary afferent neurons, the underlying molecular and cellular mechanisms remain unclear. In this study, we identified a novel functional role of the 5-HT1D receptor subtype in regulating A-type potassium (K+) currents (I-A) as well as membrane excitability in small trigeminal ganglion (TG) neurons. We found that the selective activation of 5-HT1D, rather than 5-HT1B, receptors reversibly increased I-A, while the sustained delayed rectifier K+ current was unaffected. The 5-HT1D-mediated IA increase was associated with a depolarizing shift in the voltage dependence of inactivation. Blocking G-protein signaling with pertussis toxin or by intracellular application of a selective antibody raised against G alpha. or G beta abolished the 5-HT1D effect on I-A. Inhibition of protein kinase A (PICA), but not of phosphatidylinositol 3-kinase or protein kinase C, abolished the 5-HT1D-mediated I-A increase. Analysis of phospho-p38 (p-p38) revealed that activation of 5-HT1D, but not 5-HT1B, receptors significantly activated p38, while p-ERK and p-JNK were unaffected. The p38 MAPK inhibitor SB203580, but not its inactive analogue SB202474, and inhibition of B-Raf blocked the 5-HT1D-mediated IA response. Functionally, we observed a significantly decreased action potential firing rate induced by the 5-HT1D receptors; pretreatment with 4-aminopyridine abolished this effect. Taken together, these results suggest that the activation of 5-HT1D receptors selectively enhanced I-A via the Gm, of the G omicron.-protein, PICA, and the sequential B-Raf-dependent p38 MAPK signaling cascade. This 5-HT1D, receptor effect may contribute to neuronal hypoexcitability in small TG neurons. (C) 2016 Elsevier Inc. All rights reserved. |
| WOS标题词 | Cell Biology |
| 学科主题 | Cell Biology |
| 语种 | 英语 |
| WOS记录号 | WOS:000378670900020 |
| 源URL | [http://ir.sibs.ac.cn/handle/331001/4011]  |
| 专题 | 上海神经科学研究所_神经所(总) |
| 推荐引用方式 GB/T 7714 | Zhao, XY,Zhang, Y,Qin, WJ,et al. Serotonin type-1D receptor stimulation of A-type K+ channel decreases membrane excitability through the protein kinase A- and B-Raf-dependent p38 MAPK pathways in mouse trigeminal ganglion neurons[J]. CELLULAR SIGNALLING,2016,28(8):979-988. |
| APA | Zhao, XY.,Zhang, Y.,Qin, WJ.,Cao, JP.,Zhang, Y.,...&Tao, J.(2016).Serotonin type-1D receptor stimulation of A-type K+ channel decreases membrane excitability through the protein kinase A- and B-Raf-dependent p38 MAPK pathways in mouse trigeminal ganglion neurons.CELLULAR SIGNALLING,28(8),979-988. |
| MLA | Zhao, XY,et al."Serotonin type-1D receptor stimulation of A-type K+ channel decreases membrane excitability through the protein kinase A- and B-Raf-dependent p38 MAPK pathways in mouse trigeminal ganglion neurons".CELLULAR SIGNALLING 28.8(2016):979-988. |
入库方式： OAI收割
来源：上海神经科学研究所
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