摘要
目的 研究溴氰菊酯对大鼠神经细胞内游离钙 ([Ca2 +]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 80 1、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～ 2 0 0nmol 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 0 1) ,并有良好的剂量 反应关系 (相关系数分别为r =0 96 4,r =0 981) ;AP5、MK 80 1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。
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.
出处
《卫生毒理学杂志》
CAS
CSCD
北大核心
2001年第4期216-219,共4页
Journal of Health Toxicology
基金
国家自然科学基金重点课题 (№ 39430 110 )
