皮质神经元网络同步自发钙振荡的特性  

The property of synchronized Ca^(2+) spikes in cultured cortical networks

作　　者：贺军[1] 林莉[1] 杨世民[1] 李和[1] 

机构地区：[1]华中科技大学同济医学院,武汉430030

出　　处：《华中师范大学学报（自然科学版）》2008年第3期404-408,414,共6页Journal of Central China Normal University：Natural Sciences

基　　金：教育部博士点基金项目(20070487184);湖北省自然科学基金项目(16510012)

摘　　要：通过实验证实培养的皮质神经元网络存在一种同步自发钙振荡.这种钙振荡是突触活动驱动的,可以被TTX,谷氨酸受体拮抗剂CNQX/APV所阻断.而GABAA受体阻断剂picrotoxin对其没有影响,表明这种自发钙振荡完全依赖于谷氨酸能突触活动.同样证实这种同步自发钙振荡依赖于外钙的内流,而不需要胞内钙库钙的释放,L型钙通道阻断剂nifedipine完全阻断这种自发钙振荡,表明钙的内流主要通过L型钙通道.This paper demonstrate that cortical neurons in dissociated cultures exhibited synchronized spontaneous Ca^2＋ spikes. The synchronized spontaneous Ca^2＋ spikes are synaptically driven, as it is blocked by tetrodotoxin, and by the glutamate receptor antagonist CNQX/APV. The oscillatory activity is not influenced by GABAA receptor antagonist picrotoxin, suggesting that they entirely rely on glutamatergic neurotransmission. We have also found that these Ca^2＋ spikes are dependent on an influx of extracellular Ca^2＋ but are independent of mobilization of Ca^2＋ from intracellular Ca^2＋ stores. Ca^2＋ entry occurred primarily through L-type voltage-gated calcium channels, since nifedipine completely blocked these Ca^2＋ spikes.

关 键 词：同步自发钙振荡 发生机制 L型钙通道 

分 类 号：O614.23[理学—无机化学]