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目的阐明一氧化氮（ｎｉｔｒｉｏｘｉｄｅ，ＮＯ）在青霉素致痫中的作用及与ＮＭＤＡ及非ＮＭＤＡ受体的关系。方法用自制的一氧化氮敏感电极——Ｎａｆｉｏｎ－壳聚糖合镍修饰铂电极（Ｎａｆｉｏｎ－ＣＴＳ（Ｎｉ）－Ｐｔ）连续测定了青霉素致痫海马脑片ＣＡ１区锥体层神经元ＮＯ的释放，并同时观察了Ｎ－ｍｅｔｈｙｌ－Ｄ－ａｓｐａｒａｔｅ（ＮＭＤＡ）受体阻断剂ＤＬ－２－ａｍｉｎｏ－ｐｈｏｓｐｈｏ－ｎｏ－ｖａｌｅｒｉｃａｃｉｄ（ＡＰ５）及非ＮＭＤＡ／ＡＭＰＡ受体阻断剂６，７－ｄｉｎｉ－ｔｒｏｑｕｉｎｏｘａｌｉｎｅ－２，３（１ｈ，４ｈ）－ｄｉｏｎｅ（ＤＮＱＸ）对诱发痫波及ＮＯ含量的影响。结果①自制ＮＯ敏感电极检测ＮＯ浓度线性范围为４．５×１０－４～１．０×１０－８ｍｏｌ·Ｌ－１，检测下限为５．０×１０－８ｍｏｌ·Ｌ－１；②青霉素致痫时ＮＯ释放增加，与诱发脑片痫波有剂量反应关系；③ＮＭＤＡ受体阻断剂ＡＰ５（５０μｍｏｌ·Ｌ－１）明显抑制电刺激Ｓｃｈａｆｅｒ＇ｓ纤维引起的ＣＡ１区诱发痫波，表现为痫波数减少，同时伴有ＮＯ释放下降；④非ＮＭＤＡ受体阻断剂ＤＮＱＸ（３μｍｏｌ·Ｌ－１）对诱发痫波作用不明显，ＮＯ释放亦无显著变化；⑤ＡＰ５与一氧化?
Objective To elucidate the role of nitric oxide (NO) in the development of penicillin-induced epilepsy and its relationship with NMDA and non-NMDA receptors. Methods The nitric oxide sensitive electrode - Nafion-CTS (Ni) -Pt) was used to determine the NO release from pyramidal neurons in CA1 area of penicillin-induced epileptic hippocampal slices The effects of N-methyl-D-asparate (NMDA) receptor blocker DL-2-amino-phospho-no-valericacid (AP5) and non-NMDA / AMPA receptor blockers 6,7-dini- Effect of troquinoxaline-2,3 (1h, 4h) -dione (DNQX) on evoked wave and NO content. Results ① The linear range of NO concentration was 4.5 × 10-4 ~ 1.0 × 10-8 mol·L-1 and the detection limit was 5.0 × 10-8 mol·L-1. Epileptic NO release increased, and the induced brain slices of epileptic wave dose-response relationship; ③ NMDA receptor antagonist AP5 (50μmol·L-1) significantly inhibited Schafer’s fiber-induced CA1 area induced epileptiform waves, showing epilepsy Wave number decreased, accompanied by decreased NO release; ④ DNQX (3μmol·L-1), a non-NMDA receptor antagonist, had no obvious effect on the induced epileptic wave and no significant change of NO release;