The sensation of pain is critical for the survival of animals and humans. However, the brain mechanisms underlying pain perception remain largely unknown. How does the brain decode the pain-evoked activity into a particular sensory experience？ Over the past decade, attempts have been made to answer these questions by employing electrophysiological, functional brain imaging, and behavioral approaches, and some basic properties of pain formation have been revealed. Researchers have gradually recognized that there exists a distributed neural network that participates in the transmission and processing of pain information. These studies will further guide the development of more effective treatment for many disorders such as chronic pain.
目的采用电生理记录和行为学观察研究了外周初级传入神经元对单独和联合使用ATP及缓激肽(BK)的反应及其机制。方法在大鼠新鲜分离背根神经节(DRG)神经元标本上应用全细胞膜片钳技术记录ATP激活电流(I_(ATP))以及BK对I_(ATP)的调制作用,并结合痛行为实验进行整体行为观察。结果在大鼠新鲜分离的DRG细胞上预加BK后再加ATP,则I_(ATP)明显增强,其增强程度依赖于BK的浓度(10^(-6)～10^(-4) mol/L)。预加BK后ATP的量—效曲线上移,其电流最大值与对照相比增加20.75%,而BK预加前后ATP量—效曲线的EC_(50)值非常接近(1.65×10^(-5)(?) 2.0×10^(-5)mol/L)。在大鼠后肢掌底皮下分别注射BK和ATP均引起浓度依赖性的痛行为(抬腿)反应.当联合应用BK(10^(-6)mol/L)和ATP(10^(-5),10^(-4) and 10^(-3)mol/L)时,后爪抬腿时间随ATP浓度的增大而急剧地增强。结论炎性介质BK、ATP等在外周感觉神经来梢疼痛信息的产生、传递和调制方面起着重要的作用。ATP和BK具有协同作用,这种作用是非竞争性的,BK能明显增强I_(ATP)预加BK后,随着ATP浓度的增高所诱导的痛行为反应急剧增加。
目的 观察川芎嗪(TMP)对嘌呤2 X(P2 X)受体激动剂[三磷酸腺苷(ATP)和α,β-亚甲三磷酸腺苷(α,β- me ATP) ]、前列腺素E2 (PGE2 )及P物质(SP)所致大鼠足底急性伤害性反应的影响。方法 通过大鼠痛行为反应确定局部应用TMP对ATP等P2 X受体激动剂、PGE2 及SP所致大鼠足底急性伤害性反应和足底炎症水肿的影响。结果 TMP (10 mm ol/L )明显抑制ATP (1μm ol/L )或α,β- m e ATP (0 .6μm ol/L )引起的大鼠足底急性伤害性反应。TMP(10 m mol/L)可抑制PGE2 (5 μmol/L)或α,β- me ATP(0 .2 μm ol/L)加PGE2 (5 μmol/L )引起的伤害性反应。TMP (10 m mol/L )不影响α,β- me ATP (0 .2μmol/L )加SP (10μmol/L )引起的伤害性反应。TMP对PGE2 、SP或α,β- m e ATP分别加PGE2 或SP引起的大鼠足底炎症水肿无明显影响。结论 TMP主要通过抑制P2 X受体兴奋介导的伤害性信息传递产生抗伤害性反应作用。
