ATP对大鼠三叉神经节小直径神经元胞内钙浓度的调制作用及其机制

目的探讨神经递质ATP通过何种途径引起大鼠三叉神经节(trigeminal ganglion,TG)小直径神经元胞内钙离子浓度升高。方法在急性分离的TG神经元上,应用钙离子成像技术检测胞内游离Ca2+浓度(Ca2+]i)的变化。结果在大鼠TG小直径神经元中,ATP(100μmol·L-1),thap-sigargin(1μmol·L-1,内质网钙泵抑制剂)和咖啡因(20mmol·L-1,内质网钙离子通道开放剂)在正常细胞外液和去除细胞外Ca2+的情况下,均能够引起细胞Ca2+]i升高。在细胞外无Ca2+条件下,thapsigargin能够可逆地抑制ATP引起细胞内Ca2+]i升高(n=8,P<0.01),而咖啡因对ATP引起的细胞内Ca2+]i升高无影响(n=6,P>0.05)。然而在正常外液中,thapsigargin不能完全抑制ATP引起的细胞内Ca2+]i升高,不过ATP引起的细胞内Ca2+]i升高的幅度明显地低于thapsigargin处理前(n=7,P<0.05)。结论在大鼠TG小直径神经元中,存在有IP3敏感钙库和Ryanod-ine敏感钙库。ATP可通过激动P2Y受体引起IP3敏感钙库的Ca2+释放,也可通过激动P2X受体引起细胞外钙内流。

ATP-induced intracellular calcium signal transduction mechanism in the small trigeminale ganglion neurons of rat

Aim To discuss how the neurotransmitter ATP triggers intracellular Ca2+ concentration (Ca2+]i) rise in the small trigeminale ganglion(TG) neurons of rat.Method In acutely isolated TG neurons,calcium imaging technique was applied to monitor the change ofCa2+]i.Results In the small trigeminale ganglion(TG) neurons of rat,ATP (100 μmol · L-1),as well as thapsigargin(1 μmol·L-1),a sarcoplasmic reticulum Ca2+ pump ATPase inhibitor,and caffeine (20 mmol · L-1),a sarcoplasmic reticulum Ca2+ channel opener,could induceCa2+]irise in normal extracellular solution or Ca2+-free extracellular solution.In Ca2+-free extracellular solution,the ATP-in-ducedCa2+ ]irise was reversibly inhibited by thapsigargin(n=8,P<0.01),but was not affected by caffeine(n=6,P>0.05).In normal extracellular solution,the ATP-inducedCa2+]itransients were partly inhibited by thapsigargin(n=7,P<0.05).Conclusions Both IP3-sensitivity Ca2+ stores and ryanodine-sensitivity Ca2+ stores exist in small TG neurons of rat.ATP can trigger Ca2+ release from IP3-sensitivity Ca2+ stores via activating P2Y receptors,and also can induce extracellular Ca2+ influx through P2X receptors.