Ketogenic diet protects against epileptogenesis as well as neuronal loss in amygdaloid-kindling seizures

Ketogenic diet protects against epileptogenesis as well as neuronal loss in amygdaloid-kindling seizures
复制标题

生酮饮食可预防癫痫发生以及杏仁核引发癫痫发作时的神经元损失

DOI:
10.1016/j.neulet.2011.12.002
复制
发表时间:
2012-02-02
影响因子:
2.5
通讯作者:
Ding, Mei-Ping
Ding, Mei-Ping
中科院分区:
医学4区
文献类型:
--
作者:
Jiang, Yan;Yang, Yi;Ding, Mei-Ping

文献摘要

被引文献

相似文献

生酮饮食(KD)在几个实验模型中显示出抗惊厥和抗癫痫特性方面的有益作用。然而,很少有研究调查KD的后果,在点燃诱导的癫痫发作的抗癫痫和神经保护作用。在此,出生后第28天的雄性Sprague-Dawley大鼠接受两种实验饮食之一,持续4周:(a)“经典”4:1 KD;和(B)正常的常规啮齿动物食物饮食(ND)。完全点燃癫痫发作是通过每天电刺激杏仁核来实现的。每天评估癫痫发作阶段和出院后持续时间(ADD)。每5天测量一次后放电阈值(ADT)。采用尼氏染色法观察点燃前和刺激后20天两种饮食对神经元丢失的影响。我们发现KD延迟了癫痫发作阶段和ADD的进展。KD在第5天阻止ADT降低。MD组全身性癫痫发作的发生率低于ND组。KD组点燃前同侧齿状回门区、CA 1区及对侧CM区神经元密度降低。然而,MD防止神经元的损失在同侧CA 1区刺激后20天。我们的数据表明,KD可以通过防止点燃癫痫发作中后放电的产生和传播来防止癫痫发生。此外,尽管MD改变了生命早期海马的发育,但它在点燃过程中也具有神经保护功能。(C)2011爱思唯尔爱尔兰有限公司保留所有权利。
Ketogenic diets (KD) have shown beneficial effects in terms of anticonvulsant and anti-epileptogenic properties in several experimental models. However, few studies have investigated the consequences of KD with regards to the anti-epileptogenic and neuroprotective effects in kindling-induced seizures. Here, postnatal day 28 male Sprague-Dawley rats received one of two experimental diets for 4 weeks: (a) a 'classic' 4:1 KD; and (b) a normal regular rodent chow diet (ND). Fully-kindled seizures were achieved by daily electrical stimulation in the amygdala. Seizure stage and after-discharge duration (ADD) were assessed daily. The after-discharge threshold (ADT) was measured every 5 days. The effects of the two diets on neuronal loss were observed before kindling and 20 days after stimulation by Nissl staining. We found that the progression of seizure stage and ADD was delayed by KD. KD prevented the ADT decrease on day 5. The incidence of generalized seizures was lower in the MD group compared to the ND group. The neuronal density was decreased in the ipsilateral hilus of the dentate gyrus (DG) and CA1 area, as well as the contralateral CM area before kindling in the KD group. However, MD prevented neuronal loss in the ipsilateral CA1 area 20 days after stimulation. Our data suggest that KD can protect against epileptogenesis by preventing both after-discharge generation and propagation in kindling seizures. In addition, MD also possesses a neuroprotective function during kindling although it changes hippocampal development in early life. (C) 2011 Elsevier Ireland Ltd. All rights reserved.