摘要
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。
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 of[Ca2＋]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 induce[Ca2＋]irise in normal extracellular solution or Ca2＋-free extracellular solution.In Ca2＋-free extracellular solution,the ATP-in-duced[Ca2＋ ]irise was reversibly inhibited by thapsigargin（n=8,P0.01）,but was not affected by caffeine（n=6,P0.05）.In normal extracellular solution,the ATP-induced[Ca2＋]itransients were partly inhibited by thapsigargin（n=7,P0.05）.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.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2010年第11期1450-1454,共5页
Chinese Pharmacological Bulletin
基金
国家自然科学基金资助项目(No30670694)
安徽省教育厅自然科学研究基金资助项目(No2006KJ361B)
安徽医科大学博士科研启动基金资助项目(NoXJ2005006)
上海市博士后科研基金资助项目(No10R21415000)
