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首页> 外文期刊>The European Journal of Neuroscience >The role of nitric oxide in glutaric acid-induced convulsive behavior in pup rats
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The role of nitric oxide in glutaric acid-induced convulsive behavior in pup rats

机译：一氧化氮在幼虫酸诱导的尿酸诱导的腹腔腺症中的作用

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摘要

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 mu l, 1.3 mu mol/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 precursorl-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.
机译：戊二酸血症I型（GA-I）是一种以戊二酸（GA）累积和癫痫发作为特征的脑器质性疾病。由于GA-I患儿癫痫发作加剧，且该疾病的机制尚未完全确定，我们决定研究一氧化氮（NO）在GA诱导的幼鼠惊厥行为中的作用。麻醉幼鼠雄性Wistar大鼠（18日龄）并将其置于立体定向仪中，以便将套管插入纹状体以注射GA。实验在手术后3天进行（幼鼠21日龄）。纹状体内注射GA（1μl，1.3μmol/纹状体）或生理盐水前30分钟，腹腔注射NO合成抑制剂（N-G-硝基-l-精氨酸甲酯-l-NAME，40 mg/kg）或生理盐水（载体）。纹状体内注射后，立即记录20分钟的癫痫发作潜伏期和持续时间。在幼鼠中，服用L-NAME显著增加了第一次癫痫发作的潜伏期，并缩短了GA诱导的癫痫发作持续时间。给予NO前体精氨酸（L-ARG；80 mg/kg）可预防L-NAME的作用。此外，GA显著增加幼鼠纹状体中的硝酸盐和亚硝酸盐（NOx）水平，且预给药L-NAME阻止了这种改变。L-ARG阻断了L-NAME引起的纹状体NOx的减少。这些结果是实验证据，证明NO在GA诱导的幼鼠癫痫发作中起作用，对于理解这种有机酸血症儿童神经症状的生理病理学和开发新的治疗策略具有价值。

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