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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。
OBJECTIVE: To investigate the response of peripheral primary afferent neurons to ATP and bradykinin (BK) alone and in combination with electrophysiological recording and behavioral observation. Methods Whole-cell patch-clamp technique was used to record ATP-activated currents (I ATP) and BK modulation of I ATP in freshly isolated DRG neurons in rats. Combined with pain behavior experiments Overall behavior observation. RESULTS: After pretreatment with BK and ATP in freshly isolated rat DRG cells, the I (ATP) increased markedly, and the degree of enhancement was dependent on the concentration of BK (10 -6 to 10 -4 mol / L). The pretreatment BK increased the ATP-uptake curve and increased the maximum current by 20.75% compared with the control, while the EC 50 value of the ATP volume-response curve before and after pretreatment with BK was very close to 1.65 × 10 ~ (-1) 5) (?) 2.0 × 10 ~ (-5) mol / L). BK and ATP were injected subcutaneously in the hindlimb of rats' hind limbs to induce concentration-dependent painful leg reaction.When combined with 10 ~ (-6) mol / L BK and 10 ~ (-5) , 10 ~ (-4) and 10 ~ (-3) mol / L), the time of raising the hind paw sharply increased with the increase of ATP concentration. Conclusion The inflammatory mediators such as BK and ATP play an important role in the generation, transmission and modulation of peripheral sensory nerve head pain information. ATP and BK have a synergistic effect. This effect is noncompetitive. BK can significantly increase the pre-BK IK, and the pain response induced by the increase of ATP concentration increases sharply.