中文摘要：

目的探讨糖皮质激素（GC）对大鼠杏仁核神经元凋亡的影响。方法原代培养大鼠杏仁核神经元,首先采用免疫荧光技术对培养的原代神经元及其是否存在丰富的糖皮质激素受体分别进行了鉴定,并用流式细胞术检测不同浓度的人工合成糖皮质激素地塞米松（10^-9-10^-6mol·L^-1）对杏仁核神经元细胞凋亡的影响。然后将实验分为4组：对照组（CON）、地塞米松（DEX）刺激组、地塞米松和米非司酮（受体抑制剂）共同刺激组（DEX＋MIF）、米非司酮刺激组（MIF）。用TUNEL原位技术检测各组的凋亡情况,并用RTPCR技术检测各组Bax mRNA的表达变化。结果 （1）与CON组相比,不同浓度的DEX作用于神经元后,神经元凋亡率明显升高（P〈0.05）,且呈浓度依赖性;（2）TUNEL染色结果显示,DEX组细胞凋亡率明显高于CON组（P〈0.05）,而与DEX组相比,DEX＋MIF组凋亡率明显降低（P〈0.05）,MIF组与CON组相比无明显差异（P〉0.05）;（3）与CON组相比,DEX组Bax mRNA的表达量明显升高（P〈0.05）,而与DEX组相比,DEX＋MIF组的Bax mRNA的表达量明显降低（P〈0.05）,MIF组与CON组相比无明显差异（P〉0.05）。结论糖皮质激素可以通过其受体诱导大鼠原代培养杏仁核神经元的凋亡。

英文摘要：

Aim To investigate the role of GC in inducing apoptosis of amygdaloid neurons. Methods Culturing primary neurons of amygdala,the neurons were identified by immunefluorescence techniques with antibody against microtubule associated protein-2（ MAP2）and antibody against GC receptor. Using flow cytometry to detect the effects of different concentrations of dexamethasone on the amygdala neuron apoptosis.Then the experiment was divided into four groups：CON,DEX,DEX ＋ MIF and MIF. The rate of apopto-sis of the four groups was detected by TUNEL technique and the expressions of BAX mRNA of four groups by Real-time PCR technique. Results（ 1）Compared with the control group,the percentage of apoptotic cells increased significantly with DEX（ 10^-8mol·L^-1- 10^-6mol·L^-1） treatment in a concentration-dependent manner.（ 2） the TUNEL test showed that the percentage of apoptotic cells of DEX group increased significantly, compared with control group.While it decreased significantly in DEX ＋ MIF group,compared with DEX group. There was no differencebetween MIF group and control group.（ 3） Compared with control group,the expressions of BAX mRNA of DEX group increased significantly. While the expressions of BAX mRNA of DEX ＋ MIF group decreased significantly,compared with the DEX group. There was no difference between MIF group and control group.Conclusion GC can independently induce the apoptosis of primary cultured neurons in the amygdala by combining with GC receptor.