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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Ketogenic diet is antiepileptogenic in pentylenetetrazole kindled mice and decrease levels of N-acylethanolamines in hippocampus.
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Ketogenic diet is antiepileptogenic in pentylenetetrazole kindled mice and decrease levels of N-acylethanolamines in hippocampus.

机译：生酮饮食在戊四唑点燃的小鼠中具有抗癫痫作用，可降低海马中N-酰基乙醇胺的水平。

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The ketogenic diet (KD) is used for the treatment of refractory epilepsy in children, however, the mechanism(s) remains largely unknown. Also, the antiepileptogenic potential in animal models of epilepsy has been poorly addressed. Activation of cannabinoid type-1 receptor (CB(1)-R) upon seizure activity may mediate neuroprotection as may several N-acylethanolamines. It is unknown how the KD interfere with the endocannabinoid system. We investigated the antiepileptogenic potential of the KD in the pentylenetetrazole kindling model in young mice and measured the hippocampal levels of CB(1)-R by Western blot and of endocannabinoids and N-acylethanolamines by mass spectrometry. The KD significantly decreased incidence and severity of seizures, and significantly increased the latency to clonic convulsions. There were no changes in levels of endocannabinoids or CB(1)-R expression by either seizure activity or type of diet. The level of oleoylethanolamide as well as the sum of N-acylethanolamines were significantly decreased by the KD, but were unaffected by seizure activity. The study shows that the KD had clear antiepileptogenic properties in the pentylenetetrazole kindling model and does not support a role of endocannabinoids in this model. The significance of the decreased hippocampal level of oleoylethanolamide awaits further studies.
机译：生酮饮食（KD）用于治疗儿童难治性癫痫，但是，其机制仍然未知。同样，在癫痫动物模型中抗癫痫的潜力还没有得到很好的解决。癫痫发作时激活大麻素1型受体（CB（1）-R）可能会介导神经保护，就像几种N-酰基乙醇胺一样。尚不知道KD如何干扰内源性大麻素系统。我们调查了幼鼠戊四氮点燃模型中KD的抗癫痫发生潜力，并通过Western印迹法测定了海马CB（1）-R的水平，并通过质谱法测定了海马中的大麻素和N-酰基乙醇胺的水平。 KD显着降低了癫痫发作的发生率和严重程度，并显着增加了阵挛性抽搐的潜伏期。癫痫发作活动或饮食类型对内源性大麻素或CB（1）-R表达水平没有影响。 KD显着降低了油酰基乙醇酰胺的水平以及N-酰基乙醇胺的总量，但不受癫痫发作活动的影响。研究表明，KD在戊四唑点燃模型中具有明显的抗癫痫发生特性，并且不支持内源性大麻素在该模型中的作用。降低的海马油酰乙醇酰胺水平的意义尚待进一步研究。

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