溴氰菊酯对大鼠神经细胞内游离钙的影响

目的 研究溴氰菊酯对大鼠神经细胞内游离钙([Ca^2 ]i)的影响，并探讨其可能机制。方法 用溴氰菊酯处理分离的大鼠脑细胞，用Fura-2/AM为细胞内钙离子荧光指示剂，测定神经细胞内游离钙浓度；并利用NMDA受体竞争性拮抗剂AP5、非竞争性拮抗剂MK－801、Na^ 离子通道阻断剂TTX、电压依赖性钙通道阻断剂尼莫地平，探讨了溴氰菊酯影响胞内钙的可能机制；另外还观察了去除胞外钙时溴氰菊酯对胞内钙的影响情况。结果 溴氰菊酯浓度在0－200nmol/L范围内，可以显著提高大鼠皮层和海马细胞内游离钙的浓度（P＜0．01），并有良好的剂量－反应关系（相关系数分别为r=0.964,r=0.981);AP5、MK－801和TTX可以有效阻断溴氰菊酯的升钙作用；而尼莫地平则无影响；去除胞外钙时，溴氰菊酯的升钙作用也消失。结论 溴氰菊酯导致的胞内钙升高，主要是由谷氨酸激活NMDA受体门控钙通道引起的胞外钙内流，和电压依赖性钙通道及胞内钙库释放无关。

Effect of deltamethrin on intracellular free Ca2 + concentration in rat neural cells

Objective To study the effect of deltamethrin(DM) on intracellular free Ca 2 concentration([Ca 2 ] i)in rat neural cells as well as the possible mechanism.Methods The [Ca 2 ] i of neural cells from acute dissociated cerebral cortex and hippocamous was detected with the application of fluorescence spectrophotometry using the Ca 2 indicator Fura 2/AM.The possible mechanism by which DM alters the [Ca 2 ] i was explored by means of NMDA competitive and non competitive antagonist (AP 5 and MK 801),voltage dependent sodium channel blocker(tetrodotoxin,TTX),voltage dependent Ca 2 channel blocker(Nimodipine,NIM),respectively.The change of [Ca 2 ] i was also observed when moving out the extracellular Ca 2 .Results DM could sharply increased [Ca 2 ] i in neural cells from cerebral cortex and hippocampus when the dosage of DM from 0 nmol/L to 200nmol/L( P <0 01),and there was a positive relationship between the level of [Ca 2 ] i and the DM dosage (r=0 964 and r=0 981,respestively).The action of DM increasing [Ca 2 ] i coluld be completely blocked by AP 5,MK 801 and TTX,but NIM had no influence on [Ca 2 ] i;It was found that DM could not increase [Ca 2 ] i when moving out the extracellular Ca 2 .Conclusion The action of DM increasing [Ca 2 ] i correlated mainly with influx of extracellular Ca 2 due to the open of ligand gated Ca 2 channels which was activated by glutamate,not with the voltage gated Ca 2 channels and the release from internal Ca 2 stores.