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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.
Objective: To study the interaction between Som and GABA in brain and its relationship with pain modulation.Methods: Radioimmunoassay, amino acid analyzer and pain threshold were used.Results: Som 10 μg icv GABA content decreased significantly from 2.3 ± 0.3 and 2.2 ± 0.4 μmol g ~ (-1) to 1.6 ± 0.4 and 1.5 ± 0.2 μmol g ~ (-1) respectively in the control group. The pain threshold was increased from 4.2 ± 0.2 s increased to 7.0 ± 1.1 s.After 600 μg icv of cysteamine decreased brain Som, the content of GABA in the hippocampus and brainstem also decreased obviously, but the pain threshold remained unchanged.While GABA 1500 μg icv did not change obviously, However, Som levels in the hippocampus and brainstem decreased significantly from 55 ± 4 and 84 ± 4 ng g ~ (-1) to 37 ± 5 and 55 ± 6 ng g ~ (-1) in the control group Can be blocked by 10 μg of bicuculline, and the content of Som in the hippocampus and brainstem was significantly decreased by isoniazid 300 mg kg -1 (P <0.05) .Conclusion: There is a relationship between Som and GABA in the brain Inhibit each other, but not with their role in pain modulation.