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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。
Objective To explore the mechanism by which neurotransmitter ATP leads to the increase of intracellular calcium concentration in small diameter neurons of trigeminal ganglion (TG) in rats. Methods The changes of intracellular free Ca2 + concentration ([Ca2 +] i) in acutely isolated TG neurons were detected by calcium ionography. Results In rat TG small diameter neurons, ATP (100μmol·L-1), thap-sigargin (1μmol·L-1, ERG inhibitor) and caffeine (20mmol·L-1, Ca (superscript 2 +) - Ca (superscript 2 +) channel opener, both in normal extracellular fluid and extracellular Ca2 + removal, could induce the elevation of cellular [Ca2 +] i. In the absence of extracellular Ca2 +, thapsigargin reversibly inhibited the increase of [Ca2 +] i in cells (n = 8, P <0.01), while caffeine had no effect on the increase of intracellular [Ca2 +] i induced by ATP (n = 6, P> 0.05). However, thapsigargin did not completely inhibit the intracellular [Ca2 +] i increase induced by ATP in normal external fluids, but the increase in intracellular [Ca2 +] i induced by ATP was significantly lower than that before thapsigargin treatment (n = 7, P <0.05). Conclusion There are IP3-sensitive and Ryanod-ine-sensitive calcium stores in rat TG diameter neurons. ATP induces Ca2 + release from IP3-sensitive calcium stores by agonizing P2Y receptors and also induces extracellular calcium influx through activation of P2X receptors.