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首页> 外文期刊>The Korean Journal of Physiology & Pharmacology >Kainic Acid-induced Neuronal Death is Attenuated by Aminoguanidine but Aggravated by L-NAME in Mouse Hippocampus
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Kainic Acid-induced Neuronal Death is Attenuated by Aminoguanidine but Aggravated by L-NAME in Mouse Hippocampus

机译：海藻酸诱导的神经元死亡被氨基胍减少，但在小鼠海马中被L-NAME加重。

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摘要

Nitric oxide (NO) has both neuroprotective and neurotoxic effects depending on its concentration and the experimental model. We tested the effects of NG-nitro-L-arginine methyl ester (L-NAME), a nonselective nitric oxide synthase (NOS) inhibitor, and aminoguanidine, a selective inducible NOS (iNOS) inhibitor, on kainic acid (KA)-induced seizures and hippocampal CA3 neuronal death. L-NAME (50 mg/kg, i.p.) and/or aminoguanidine (200 mg/kg, i.p.) were administered 1 h prior to the intracerebroventricular (i.c.v.) injection of KA. Pretreatment with L-NAME significantly increased KA-induced CA3 neuronal death, iNOS expression, and activation of microglia. However, pretreatment with aminoguanidine significantly suppressed both the KA-induced and L-NAME-aggravated hippocampal CA3 neuronal death with concomitant decreases in iNOS expression and microglial activation. The protective effect of aminoguanidine was maintained for up to 2 weeks. Furthermore, iNOS knockout mice (iNOS-/-) were resistant to KA-induced neuronal death. The present study demonstrates that aminoguanidine attenuates KA-induced neuronal death, whereas L-NAME aggravates neuronal death, in the CA3 region of the hippocampus, suggesting that NOS isoforms play different roles in KA-induced excitotoxicity.
机译：一氧化氮（NO）具有神经保护作用和神经毒性作用，具体取决于其浓度和实验模型。我们测试了非选择性一氧化氮合酶（NOS）抑制剂NG-硝基-L-精氨酸甲酯（L-NAME）和选择性诱导型NOS（iNOS）抑制剂氨基胍对海藻酸（KA）诱导的影响癫痫发作和海马CA3神经元死亡。在脑室内（i.c.v.）注射KA前1小时施用L-NAME（50 mg / kg，腹腔内）和/或氨基胍（200 mg / kg，腹腔内）。用L-NAME预处理显着增加KA诱导的CA3神经元死亡，iNOS表达和小胶质细胞活化。但是，用氨基胍预处理可显着抑制KA诱导的和L-NAME加重的海马CA3神经元死亡，同时iNOS表达和小胶质细胞活化减少。氨基胍的保护作用可维持长达2周。此外，iNOS基因敲除小鼠（iNOS -/-）对KA诱导的神经元死亡具有抵抗力。本研究表明，氨基胍可减轻海马CA3区KA诱导的神经元死亡，而L-NAME加重神经元的死亡，表明NOS亚型在KA诱导的兴奋性毒性中起不同作用。

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