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脂质介质溶解素D2抑制了大鼠初级感觉神经元中的ATP电流

Jia-Wei Hao¹, Ting-Ting Liu¹, Chun-Yu Qiu¹

¹School of Pharmacy, School of Basic Medical Sciences, Xianning Medical College, Hubei University of Science and Technology, Xianning, Hubei, PR China.

Journal of neurochemistry

|November 21, 2023

概括

瑞索尔D2 (RvD2) 通过抑制感觉神经元中的P2X3受体来缓解疼痛. 这种机制涉及GPR18激活和下游信号,为疼痛管理提供了一个新的目标.

科学领域:

神经科学是一个神经科学.
药理学药理学是指药理学的学科.
分子生物学分子生物学

背景情况:

来自多可萨赫萨酸的Resolvin D2 (RvD2) 具有已知的止痛特性.
在RvD2缓解疼痛作用的基础上,精确的分子机制在很大程度上仍未被探索.

研究的目的:

为了阐明RvD2发挥其止痛作用的机制.
研究RvD2与P2X3受体及其下游信号通路在疼痛感知中的相互作用.

主要方法:

电生理学记录了大鼠背根质神经元 (DRG) 中的P2X3受体活性.
应用RvD2,α,β-甲-ATP (α,β-meATP) 和特定抗剂 (O-1918,百日咳毒素,H89) 和类似物 (8-Br-cAMP).
评估RvD2对大鼠的膜潜能,动作潜能爆发和感知行为的影响.

主要成果:

在P2X3受体中,RvD2剂量依赖地抑制了α,β-meATP诱导的向内流,减少了最大响应而不会改变亲和力.
RvD2的抑制作用是电压独立的,通过G蛋白受体18 (GPR18) 和PTX敏感的Gα_i/o-蛋白质进行介导.
在DRG神经元中,RvD2抑制了ATP触发的脱极化和动作潜能爆发,并通过外周GPR18激活在体内减弱了 nociceptive行为和allodynia.

结论:

通过一种涉及GPR18,Gα_i/o蛋白和cAMP/PKA信号的新途径,RvD2抑制了大鼠初级感觉神经元中的P2X3受体.
这项研究揭示了RvD2镇痛作用的新机制,突出了P2X3受体作为关键标.
这些发现为开发基于RvD2的疼痛管理疗法提供了基础.

关键词:

这是一个P2X3受体.在Resolvin D2中使用Resolvin D2.现在的当前流动.背部根结节神经元神经元神经元无意识的行为是有意识的行为.

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