A study on the roles of nNOS-SUMO-1 conjugation and NO-nNOS machinery in PTZ-induced convulsive seizure

我们以前报道过，在戊四唑（PTZ）诱导的鼠类广泛性癫痫模型中，神经元NO合成酶（nNOS）产生过量的一氧化氮（NO），并持续升高，这是由神经元活动异常引起的。在这项研究中，我们发现了一种新的翻译后修饰，即小泛素相关修饰物（small ubiquitin-related modifier， SUMO），它可以调节蛋白质的稳定性、活性和定位。此外，我们发现ptz诱发惊厥发作的阈值是由小鼠各脑区的NO水平决定的。

We previously reported that excessive nitric oxide (NO) was generated by neuronal NO synthase (nNOS) which is persistently increased in the generalized epilepsy model of pentylenetetrazole (PTZ)-induced kindling rodents, which is caused by abnormal neuronal activity. In this study, we characterized a novel posttranslational modification in nNOS by small ubiquitin-related modifier (SUMO) which regulates protein stability, activity and localization. In addition, we found that the threshold of PTZ-induced convulsive seizure was defined by the NO levels in various brain regions of mice.