SD大鼠红藻氨酸诱导性癫痫发作时一氧化氮合酶与γ-氨基丁酸的共同表达

根据形态学观察对一氧化氮（NO）在癫痫发作中的意义、NO与抑制性神经递质γ－氨基丁酸（GABA）的关系进行探讨．方法：选用红藻氨酸（KA）诱导的复杂部分性痫病模型．SD大鼠20只，随机分为KA30，60，90，200min组及对照组．脑组织进行还原性辅酶见依赖性黄递酶（Nd）染色，在Nd染色的基础上进行GABA免疫组织化学染色．结果：在海马CA1区、CA3区、齿状回（DG），KA建模组各时点一氧化氮合酶（NOS）与GABA双标阳性细胞数较对照组为低，具有显著性统计学差异．结论：Nd与GABA在脑内共存；GABA释放的减少导致GABA能系统解抑制；NO的释放减少，使其负反馈性抑制减弱，因而使神经元同步的阵发性放电增加．说明GABA与NO通过各自的途径起抗癫痫，也许在抗癌的发生、发展中起协同作用．

An investigation of the mechanism of coexistence of NOS with GABA during the seizure induced by kainic acid in SD rats

Objective Functional significance of NO and the relationship between NO and central inhibitory neurotransmitter GABA were investigated morphorologically. Methods: A kainate-induced complex partial seizure model was used in our experiment. Twenty SD rats were randomly divided into KA30, 60, 90, 200 min and control groups. The brain sections were stained by histochemistry for NADPH diaphorase (Nd), and were further stained for GABA by immunohistochemistry. Results: Histological and immunohistochemical study revealed that in KA groups the number of Nd positive and GABA double-labeled neurons in CA1,CA3 and dentate gyrus was significantly reduced,compared to control group. Conclusion: Nd coexisted with GABA in the brain. Reduction of GABA release led to relieve of GABA ergic inhibition and in same way, reduction of NO release decreased its negative modulatory role. Therefore neuronal synchronous paroxysmal discharge was increased. GABA and NO, both having the role of anticonvulsion,acted through different way. They perhaps function cooperatively in anticonvulsion.