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目的 观察一氧化氮 (NO)在海人酸 (KA)对脑的兴奋毒性中的作用。方法 成年雌性 Wistar大鼠双侧尾核内注射 KA。术后 3个时间点测定一氧化氮合酶 (NOS)的活性 (即测定脑匀浆加入酶反应体系中产生的 NO2 -浓度 ) ,另一批大鼠经 KA注射后第 2～ 6天每天腹腔注射 10 mg/ kg L -硝基精氨酸甲酯 (L - NAME)或 2 5 m g/ kg 7-硝基吲哚 (7- NI)。术后 10 d起进行学习记忆行为试验。结果 尾核 NOS活性在术后 6～ 8h无明显变化 ,术后 3 d显著升高 ,术后 5 d仍轻度升高。L - NAME和 7- NI都能减轻 KA所致的被动回避反应记忆损害。只有 L - NAME能改善 KA所致的主动回避反应行为缺陷。结论 进一步表明 NOS激活和过量 NO可能介导 KA的兴奋毒性。早期多次使用 NOS抑制剂对 KA兴奋毒性引起的记忆缺陷有一定的改善作用。
Objective To observe the role of nitric oxide (NO) in the excitotoxicity of kainate to brain. Methods Adult female Wistar rats were injected bilateral caudal nuclei with KA. The activity of nitric oxide synthase (NOS) was measured at 3 time points (ie, the concentration of NO2 - produced by adding brain homogenate to the enzyme reaction system). The other rats were injected daily for 2 to 6 days after KA injection Intraperitoneal injection of 10 mg / kg L - NAME or 25 mg / kg 7 - nitroindole (7 - NI). After 10 days learning and memory behavior test. Results The activity of NOS in caudate nucleus showed no significant change at 6-8 h postoperation, and increased significantly at 3 d postoperatively, but still slightly increased at 5 d postoperative. Both L - NAME and 7 - NI attenuated KA - induced passive avoidance memory impairment. Only L - NAME can improve the KA caused by active avoidance response behavioral defects. Conclusions further suggest that NOS activation and excessive NO may mediate the excitotoxicity of KA. Multiple early use of NOS inhibitors can improve memory deficits caused by KA excitotoxicity.