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The role of nitric oxide in glutaric acid-induced convulsive behavior in pup rats.
European Journal of Neuroscience ( IF 2.7 ) Pub Date : 2020-05-27 , DOI: 10.1111/ejn.14840 César Augusto Brüning 1 , Suzan Gonçalves Rosa 2 , Caroline Brandão Quines 2 , Danieli Valnes Magni 2 , Natália Tavares Nonemacher 1 , Cristiani Folharini Bortolatto 1 , Cristina Wayne Nogueira 2
European Journal of Neuroscience ( IF 2.7 ) Pub Date : 2020-05-27 , DOI: 10.1111/ejn.14840 César Augusto Brüning 1 , Suzan Gonçalves Rosa 2 , Caroline Brandão Quines 2 , Danieli Valnes Magni 2 , Natália Tavares Nonemacher 1 , Cristiani Folharini Bortolatto 1 , Cristina Wayne Nogueira 2
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Glutaric acidaemia type I (GA‐I) is a cerebral organic disorder characterized by the accumulation of glutaric acid (GA) and seizures. As seizures are precipitated in children with GA‐I and the mechanisms underlying this disorder are not well established, we decided to investigate the role of nitric oxide (NO) in GA‐induced convulsive behaviour in pup rats. Pup male Wistar rats (18‐day‐old) were anesthetized and placed in stereotaxic apparatus for cannula insertion into the striatum for injection of GA. The experiments were performed 3 days after surgery (pup rats 21‐day‐old). An inhibitor of NO synthesis (N‐G‐nitro‐l ‐arginine methyl ester—L‐NAME, 40 mg/kg) or saline (vehicle) was administered intraperitoneally 30 min before the intrastriatal injection of GA (1 µl, 1.3 µmol/striatum) or saline. Immediately after the intrastriatal injections, the latency and duration of seizures were recorded for 20 min. The administration of L‐NAME significantly increased the latency to the first seizure episode and reduced the duration of seizures induced by GA in pup rats. The administration of the NO precursor l ‐arginine (L‐ARG; 80 mg/kg) prevented the effects of L‐NAME. Besides, GA significantly increased nitrate and nitrite (NOx) levels in the striatum of pup rats and the preadministration of L‐NAME prevented this alteration. L‐ARG blocked the reduction of striatal NOx provoked by L‐NAME. These results are experimental evidence that NO plays a role in the seizures induced by GA in pup rats, being valuable in understanding the physiopathology of neurological signs observed in children with this organic acidaemia and to develop new therapeutic strategies.
中文翻译：
一氧化氮在戊二酸诱导的大鼠惊厥行为中的作用。
I型戊二酸血症（GA-I）是一种脑器质性疾病，其特征在于戊二酸（GA）积累和癫痫发作。由于GA-I患儿癫痫发作加剧，并且尚不清楚该疾病的潜在机制，因此我们决定研究一氧化氮（NO）在GA诱发幼鼠惊厥行为中的作用。麻醉幼龄Wistar雄性大鼠（18天），将其放置在立体定位仪中，以将套管插入纹状体中以注射GA。实验是在术后3天进行的（21岁的幼鼠）。NO合成（N-G-硝基的抑制剂升在纹状体内注射GA（1 µl，1.3 µmol / striatum）或生理盐水之前30分钟，腹膜内注射精氨酸甲酯-L-NAME（40 mg / kg）或生理盐水（车辆）。纹状体内注射后立即记录发作的潜伏期和持续时间，持续20分钟。L‐NAME的使用显着增加了第一次癫痫发作的潜伏期，并减少了由GA诱发幼鼠癫痫发作的持续时间。所述NO前体的给药升精氨酸（L-ARG； 80 mg / kg）可防止L-NAME的影响。此外，GA显着增加了幼鼠纹状体中硝酸盐和亚硝酸盐（NOx）的水平，而预先给予L-NAME可阻止这种变化。L‐ARG阻止了L‐NAME引起的纹状体NOx的减少。这些结果是实验证据，表明NO在幼鼠的GA诱发的癫痫发作中起作用，对于了解在这种有机酸血症儿童中观察到的神经系统体征的生理病理学以及制定新的治疗策略具有重要意义。
更新日期：2020-05-27
中文翻译：
一氧化氮在戊二酸诱导的大鼠惊厥行为中的作用。
I型戊二酸血症（GA-I）是一种脑器质性疾病，其特征在于戊二酸（GA）积累和癫痫发作。由于GA-I患儿癫痫发作加剧，并且尚不清楚该疾病的潜在机制，因此我们决定研究一氧化氮（NO）在GA诱发幼鼠惊厥行为中的作用。麻醉幼龄Wistar雄性大鼠（18天），将其放置在立体定位仪中，以将套管插入纹状体中以注射GA。实验是在术后3天进行的（21岁的幼鼠）。NO合成（N-G-硝基的抑制剂升在纹状体内注射GA（1 µl，1.3 µmol / striatum）或生理盐水之前30分钟，腹膜内注射精氨酸甲酯-L-NAME（40 mg / kg）或生理盐水（车辆）。纹状体内注射后立即记录发作的潜伏期和持续时间，持续20分钟。L‐NAME的使用显着增加了第一次癫痫发作的潜伏期，并减少了由GA诱发幼鼠癫痫发作的持续时间。所述NO前体的给药升精氨酸（L-ARG； 80 mg / kg）可防止L-NAME的影响。此外，GA显着增加了幼鼠纹状体中硝酸盐和亚硝酸盐（NOx）的水平，而预先给予L-NAME可阻止这种变化。L‐ARG阻止了L‐NAME引起的纹状体NOx的减少。这些结果是实验证据，表明NO在幼鼠的GA诱发的癫痫发作中起作用，对于了解在这种有机酸血症儿童中观察到的神经系统体征的生理病理学以及制定新的治疗策略具有重要意义。
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