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目的探讨氨基酸类及肽类神经递质的关系及各自在癫癎发生发展过程中的作用机制。方法采用戊四氮(PTZ) 制备大鼠慢性癫癎模型,应用高效液相色谱仪,结合紫外分光光度仪检测大鼠额叶皮层、海马及乳头体组织γ-氨基丁酸(GA- BA)和谷氨酸(GLU)的含量变化。采用放射免疫方法测定大鼠额叶皮层、海马及乳头体中生长抑素(SOM)含量的变化。结果GLU在腹腔注射戊四氮15 d、点燃后0 h,7、30 d组额叶皮层、海马及乳头体组织中含量显著高于对照组。GABA在腹腔注射PTZ 15 d、点燃后7、30 d组额叶皮层、海马及乳头体组织中含量明显低于对照组,而点燃后0 h组与对照组无显著差异。SOM在腹腔注射PTZ 15 d、点燃后0 h,7、30 d组额叶皮层及乳头体组织中的含量显著升高,而海马无明显变化。相关分析发现。GABA与GLU、GABA与SOM之间呈直线负相关,GLU与SOM之间呈直线正相关。结论GABA、GLU及SOM三者之间的平衡失调可能是癞癎发生的重要原因及癫癎敏感性形成的机制。乳头体及额叶皮层中SOM与癫癎发作有关,可能参与了癫癎的播散过程。
Objective To explore the relationship between amino acids and neurotransmitters and the mechanism of their action in the development of epilepsy. Methods Chronic epilepsy model was induced by pentylenetetrazole (PTZ) in rats. The contents of γ-aminobutyric acid (GA-BA) in rat cortex, hippocampus and papillary tissues were detected by high performance liquid chromatography with ultraviolet spectrophotometer. And glutamic acid (GLU) content changes. Radioimmunoassay was used to determine the content of somatostatin (SOM) in frontal cortex, hippocampus and nipple of rats. Results GLU was significantly higher in the cortex, hippocampus and nipple tissue of the frontal cortex after 15 days of pentylenetetrazol injection and 0, 7 and 30 days after ignition. The content of GABA in the cortex of the frontal cortex, hippocampus and papillary body in the PTZ group was significantly lower than that in the control group at 15 d after PTZ injection and at 7 and 30 d after ignition. There was no significant difference between the control group and the 0 h group after ignition. The content of SOM increased significantly in the cortex and papillary tissues of the frontal cortex in the PTZ group at 15 d after injection of PTZ for 15 d, but not in the hippocampus at 0 h, 7 and 30 d after ignition. Related analysis found. There was a linear negative correlation between GABA and GLU, GABA and SOM, and a linear positive correlation between GLU and SOM. Conclusions The imbalance between GABA, GLU and SOM may be the important reason for the occurrence of asthma and the mechanism of the formation of epilepsy sensitivity. SOM in the nipple and frontal cortex is associated with the onset of epilepsy and may be involved in the dissemination of epilepsy.