Substance P potentiates 5-HT3 receptor-mediated current in rat trigeminal ganglion neurons
Substance P potentiates 5-HT3 receptor-mediated current in rat trigeminal ganglion neurons
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P 物质增强大鼠三叉神经节神经元 5-HT3 受体介导的电流
DOI：
10.1016/j.neulet.2004.04.072
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发表时间：
2004-07-22
影响因子：
2.5
通讯作者：
Li, ZW
中科院分区：
文献类型：
--
作者：
Hu, WP;You, XH;Li, ZW
用全细胞膜片钳技术研究三叉神经节(TG)神经元共存的SP受体和5-HT3受体之间的相互作用。大多数神经元对5-羟色胺产生内向电流(i5-HT)(78.2%79/101)，该电流可被5-HT3受体拮抗剂ICS-205,930阻断。在大多数5-羟色胺敏感细胞(78.5%，62/79)中，预先应用SP(10(-10)~10(-8)M)可增强i5-羟色胺。联合应用SP和NK1受体拮抗剂GR-82334对I5-HT无增强作用。5-羟色胺的浓度-反应曲线显示：(1)加和不加SP的5-羟色胺的阈值浓度基本相同，而加SP使i5-羟色胺的最大值增加38.0%；(2)加和不加SP的曲线的EC50值非常接近，分别为1.89×10~(-5)M和2.08×10~(-5)M(p>；0.1；n=9)。非水解性国内生产总值类似物-β-S和选择性蛋白激酶C抑制剂GF-109203X的细胞内透析。去掉了i5-HT的SP增强作用。这些结果可能为理解由组织损伤、炎症等引起的外周疼痛的产生和/或调节的潜在机制提供线索。(C)2004年爱思唯尔爱尔兰有限公司。保留所有权利。
The present study aimed to investigate the interaction between the coexistent SP receptor and 5-HT3 receptor in trigeminal ganglion (TG) neurons using whole-cell patch clamp technique. The majority of the neurons examined responded to 5-HT with an inward current (I5-HT) (78.2% 79/101) that could be blocked by 5-HT3 receptor antagonist, ICS-205,930. The I5-HT was potentiated by preapplication of SP (10(-10) to 10(-8) M) in most 5-HT-sensitive cells(78.5%, 62/79). Coapplication of SP and GR-82334, antagonist of NK1 receptor, had no enhancing effect on I5-HT. The concentration-response curves for 5-HT with and without SP preapplication show that: (1) the threshold 5-HT concentrations with and without SP preapplication are basically the same, while SP preapplication increased the maximal value of I5-HT by 38.0% of its control: (2) the EC50 values of the curves with and without SP pretreatment are very close, i.e. 1.89 x 10(-5) M and 2.08 x 10(-5) M (p > 0.1; n = 9), respectively. Intracellular dialysis of GDP-beta-S, a non-hydrolyzable GDP analog, and GF-109203X, a selective protein kinase C inhibitor. removed the SP potentiation of I5-HT. These results may offer a clue to understanding the mechanism underlying the generation and/or regulation of peripheral pain caused by tissue damage inflammation, etc. (C) 2004 Elsevier Ireland Ltd. All rights reserved.