Department of Engineering, Trinity College, Hartford, CT 06106, USA.
J Neurophysiol. 2011 Aug;106(2):662-6. doi: 10.1152/jn.00001.2011. Epub 2011 May 25.
Ketogenic diets are very low in carbohydrates and can reduce epileptic seizures significantly. This dietary therapy is particularly effective in pediatric and drug-resistant epilepsy. Hypothesized anticonvulsant mechanisms of ketogenic diets focus on increased inhibition and/or decreased excitability/excitation. Either of these consequences might not only reduce seizures, but also could affect normal brain function and synaptic plasticity. Here, we characterized effects of a ketogenic diet on hippocampal long-term potentiation, a widely studied form of synaptic plasticity. Adult male rats were placed on a control or ketogenic diet for 3 wk before recording. To maintain the most physiological conditions possible, we assessed synaptic transmission and plasticity using chronic in vivo recordings in freely behaving animals. Rats underwent stereotaxic surgery to chronically implant a recording electrode in the hippocampal dentate gyrus and a stimulating electrode in the perforant path; they recovered for 1 wk. After habituation and stable baseline recording, 5-Hz theta-burst stimulation was delivered to induce long-term potentiation. All animals showed successful plasticity, demonstrating that potentiation was not blocked by the ketogenic diet. Compared with rats fed a control diet, rats fed a ketogenic diet demonstrated significantly diminished long-term potentiation. This decreased potentiation lasted for at least 48 h. Reduced potentiation in ketogenic diet-fed rats is consistent with a general increase in neuronal inhibition (or decrease in excitability) and decreased seizure susceptibility. A better understanding of the effects of ketogenic diets on synaptic plasticity and learning is important, as diet-based therapy is often prescribed to children with epilepsy.
生酮饮食中碳水化合物的含量非常低，可以显著减少癫痫发作。这种饮食疗法在儿科和耐药性癫痫中特别有效。生酮饮食的假设抗惊厥机制集中在增加抑制和/或减少兴奋性/兴奋上。这两种结果不仅可能减少癫痫发作，还可能影响正常的大脑功能和突触可塑性。在这里，我们描述了生酮饮食对海马长时程增强（一种广泛研究的突触可塑性形式）的影响。成年雄性大鼠在记录前接受对照或生酮饮食 3 周。为了尽可能保持最生理的条件，我们使用慢性体内记录评估了自由行为动物的突触传递和可塑性。大鼠接受立体定向手术，将记录电极植入海马齿状回，刺激电极植入穿通路径；他们恢复了 1 周。在适应和稳定基线记录后，5-Hz theta 爆发刺激被用来诱导长时程增强。所有动物都表现出成功的可塑性，表明生酮饮食没有阻断可塑性。与喂食对照饮食的大鼠相比，喂食生酮饮食的大鼠表现出明显的长时程增强减弱。这种增强的减少至少持续 48 小时。生酮饮食喂养的大鼠中增强的减少与神经元抑制的普遍增加（或兴奋性的降低）和癫痫易感性的降低一致。更好地理解生酮饮食对突触可塑性和学习的影响很重要，因为基于饮食的治疗经常被开给患有癫痫的儿童。
