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作 者:杨潇[1] 胡黔江[1] 龙景东 王高霞 曾俊伟[1] 田虹[1] 刘晓红[1]
机构地区:[1]遵义医学院基础医学院生理学教研室,遵义563000
出 处:《神经解剖学杂志》2014年第1期40-44,共5页Chinese Journal of Neuroanatomy
基 金:国家自然科学基金(30960126;31000497);遵义医学院重点学科建设项目(XZXK-20120702)
摘 要:目的:观察皮质酮(CORT)对培养的脊髓背角神经元Ca2+浓度([Ca2+]i)的调节作用及机制。方法:培养新生SD大鼠脊髓背角神经元,激光共聚焦显微镜检测神经元[Ca2+]i的变化。结果:CORT可快速升高培养的脊髓背角神经元[Ca2+]i,且呈现剂量依赖性(P<0.05);CORT诱导的神经元[Ca2+]i升高是以外钙内流为主(P<0.01);百日咳毒素(G蛋白活化阻断剂)可阻断CORT所致的脊髓背角神经元[Ca2+]i升高(P<0.01),而糖皮质激素受体拮抗剂RU38486对CORT的效应无抑制作用。结论:CORT通过非基因组途径快速增高培养的脊髓背角神经元[Ca2+]i。Objective: To explore the modulatory effects of corticosterone (CORT) on the intracellular calcium concen- tration ( [Ca2+ ]i) in cultured rat dorsal spinal neurons and the relative mechanism. Methods:Neurons from neonatal SD rat spinal cord were cultured. Confocal laser scanning microscopy were employed to detect changes of [ Ca2+ ] i in cultured neurons. Results:CORT (0.1-10 μmo]/L) caused a rapid increase in [ Ca2+ ]i with a dose-dependent manner in cul- tured dorsal spinal neurons. The action of CORT on neuronal [ Ca2+] i was blocked by pertussis toxin ( a blocker of G protein activation, 100 ng/ml) , but was unaffected by RU38486 (glueocorticoid receptor antagonist, 10 μmol/L). Con- clusion : These observations suggest that CORT can rapidly increase [ Ca2+ ] i in cultured rat dorsal spinal neurons through a nongenomic mechanism.
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