摘要
目的:研究脑内Som和GABA的相互影响及其与痛觉调制的关系.方法:应用放射免疫,氨基酸分析仪和痛阈测定法.结果:发现Som 10 μg icv可使大鼠海马,脑干内GABA含量显著减少,分别由对照组的2.3±0.3和2.2±0.4 μmol g^(-1)降至1.6±0.4和1.5±0.2μmol g^(-1),痛阈由对照组的4.2±0.2 s升高到7.0±1.1 s;半胱胺600 μg icv降低脑内Som后,海马和脑干内GABA含量也明显减少,但痛阈不变.GABA 1500 μg icv后,痛阈变化不明显,而海马、脑干内Som含量均显著减少,分别由对照组的55±4和84+4 ng g^(-1)降至37±5和55±6 ng g^(-1)这一效应可被荷包牡丹碱10 μg阻断;以异烟肼300 mg kg^(-1)降低脑内GABA后,海马和脑干内Som含量即明显增多.结论:脑内Som和GABA之间存在着相互抑制作用,但与它们在痛觉调制中的作用无关.
To study the interactive influence of so-matostatin (Som) and GABA in the brain and its relation to the pain modulation. METHOD: Using radioimmunoassay, amino acid analyzer and measurement of pain threshold. RESULTS: Som 10 μg icv increased the pain threshold (from 4. 2±0. 2 to 7.0±1. 1 s) of the rat, but reduced the content of GABA from 2. 3±0. 3 to 1. 6 ±0. 4μmol g-1 in hip-pocampus and from 2.4 ± 0. 4 to 1. 5 ± 0. 2 mmol kg-1 in brain stem. After depletion of the Som in brain by icv cysteamine (Cys, 600 μg),the content of GABA in hippocampus and brain stem was also reduced without modification of the pain threshold. GABA 1500 fxg icv had no effect on the pain threshold, however, caused a decrease of Som content from 55μ4 to 37μ5 ng g-1 in hippocampus and from 84 ± 4 to 55 ± 6 ng g-1 in brain stem, which was blocked by bicuculline (10μg) After reduced of the GABA content in brain by subcutaneous injection of isoniazid (300 mg kg-1), Som content of the hippocampus and brain stem was markedly elevated. CONCLUSION: Som and GABA inhibited each other, unrelated to their pain modulation.
出处
《中国药理学报》
CSCD
1995年第4期329-332,共4页
Acta Pharmacologica Sinica
关键词
生长抑素
氨基丁酸
痛阈
海马
脑干
somatostatin
GABA
pain reshold
hippocampus
brain stem
