Mikati Mohamad A, Injibar Hiba, Kurdi Rana M, El Hokayem Jimmy, Abou Rialy Suha, Lteif Lina, Abdul Jawad Mona, Francis Elie, Geha George, Farhat Firas
Adult and Pediatric Epilepsy Program and Department of Pediatrics, American University of Beirut, Beirut, Lebanon.
J Med Liban. 2006 Oct-Dec;54(4):200-4.
Because magnesium has antiseizure effects in some animal models of epilepsy, and possible neuroprotective effects in some models of neuronal injury, we aimed to investigate its effects in the kainic acid (KA) model of status epilepticus (SE) in prepubescent rats. This age was chosen because it is a common age for onset of epilepsy and of SE in humans. Three groups of P35 rats were studied: Group I (MgKA) received magnesium sulfate MgSO4 (270 mg/kg then 27 mg/kg every 20 minutes for 5 hours) and 10 mg/kg KA. Group II (KA) received saline instead of MgSO4 and 10 mg/kg KA. Group III (control) received saline injections only. The dose we used has been shown previously to have anticonvulsant activity in another seizure model. Rats were recorded for their acute behavioral seizures directly after KA, and underwent the handling and Morris Water Maze (MWM) tests on P96-97 and P102-106 respectively. The MgKA and the KA groups did not differ in their acute seizures and both showed similar histologic lesions in CA3/CA4 and CA1 hippocampal subfields, and were more aggressive on the handling test than control rats. The MgKA group took more time to reach the platform in MWM than controls, while the KA group scores were intermediate between the two groups. Using the dose of 540 mg/kg MgSO4 and 54 mg/kg every 20 min showed the similar result of lack of protection against impairment in long-term memory. We conclude that (1) Magnesium did not manifest acute behavioral antiseizure effects in the KA P35 model of SE. (2) Magnesium did not prevent the tested long-term behavioral and histological consequences of SE in this model.
由于镁在某些癫痫动物模型中具有抗癫痫作用,并且在某些神经元损伤模型中可能具有神经保护作用,我们旨在研究其在青春期前大鼠的海藻酸(KA)癫痫持续状态(SE)模型中的作用。选择这个年龄是因为它是人类癫痫和SE发作的常见年龄。研究了三组P35大鼠:第一组(MgKA)接受硫酸镁MgSO4(270mg/kg,然后每20分钟27mg/kg,共5小时)和10mg/kg KA。第二组(KA)接受生理盐水而非MgSO4和10mg/kg KA。第三组(对照组)仅接受生理盐水注射。我们使用的剂量先前已证明在另一种癫痫模型中具有抗惊厥活性。在注射KA后直接记录大鼠的急性行为性癫痫发作,并分别在P96 - 97和P102 - 106进行处理和莫里斯水迷宫(MWM)测试。MgKA组和KA组在急性癫痫发作方面没有差异,并且在CA3/CA4和CA1海马亚区均表现出相似的组织学损伤,并且在处理测试中比对照大鼠更具攻击性。MgKA组在MWM中到达平台的时间比对照组更长,而KA组的得分介于两组之间。使用540mg/kg MgSO4和每20分钟54mg/kg的剂量显示出类似的结果,即对长期记忆损伤缺乏保护作用。我们得出结论:(1)镁在KA P35 SE模型中未表现出急性行为抗癫痫作用。(2)镁未能预防该模型中SE所测试的长期行为和组织学后果。