Tao Tao, Chen Wei-Jie, Pan Hong-Fu, Li Bin, Liao Zhi-Gang
West China School of Preclinical and Forensic Medicine, Sichuan University, Chengdu 610041, China.
Fa Yi Xue Za Zhi. 2007 Apr;23(2):86-9.
Expressions of GABA and GABA(A)R-alpha1 in the brain of rats poisoned by Tetramine were analyzed to explore the intoxication mechanism. Methods Sixty rats were randomly divided into control, sham poisoned, high-dose poisoned (1.0 mg/kg tetramine) and low-dose poisoned (0.1 mg/kg) groups. The expressions of GABA and GABA(A)R-alpha1 in the brain of the poisoned rats were detected and analyzed by immunohistochemistry and imaging analyzer. Results The expressions of both GABA and GABA(A)R-alpha1 were diffusely seen in the brains of the control and shame poisoned rat groups with a moderate expression level, whereas the expressions of both GABA and GABA(A)R-alpha1 were decreased in the brains of the high-dose poisoned group. In the low-dose poisoned rat group, the expression of GABA initially decreased and reached its lowest level 6 hours after poisoning, and then started to show an increase and reached the level of control groups at day 3. The expressions level reached its peak at days 5-7 after poisoning and remained above the level of control groups till 10 days after poisoning. Similarly, the expression of GABA(A)R-alpha1 in the brains of the low-dose poisoned group initially decreased and reached its lowest level 6-12 hrs after poisoning, and then started to increase and reached the level of control groups at days 7-10 after poisoning, respectively. Conclusion The expression of both GABA and GABA(A)R-alpha1 decreased in the brains of the high-dose poisoned rat group and these changes of GABA and GABA(A)R-alpha1 expressions may be associated with underlying mechanism of tetramine poisoning.
分析毒鼠强中毒大鼠脑内γ-氨基丁酸（GABA）和GABA(A)R-α1的表达，以探讨中毒机制。方法将60只大鼠随机分为对照组、假中毒组、高剂量中毒组（1.0mg/kg毒鼠强）和低剂量中毒组（0.1mg/kg）。采用免疫组织化学和图像分析仪检测并分析中毒大鼠脑内GABA和GABA(A)R-α1的表达。结果对照组和假中毒组大鼠脑内GABA和GABA(A)R-α1均呈弥漫性表达，表达水平中等；高剂量中毒组大鼠脑内GABA和GABA(A)R-α1表达均降低。低剂量中毒组大鼠脑内GABA表达最初降低，中毒后6小时降至最低水平，随后开始升高，在中毒后第3天达到对照组水平。表达水平在中毒后第5 - 7天达到峰值，并在中毒后10天内一直高于对照组水平。同样，低剂量中毒组大鼠脑内GABA(A)R-α1表达最初降低，中毒后6 - 12小时降至最低水平，随后分别在中毒后第7 - 10天开始升高并达到对照组水平。结论高剂量中毒大鼠组脑内GABA和GABA(A)R-α1表达均降低，GABA和GABA(A)R-α1表达的这些变化可能与毒鼠强中毒的潜在机制有关。
