Calderón Naima, Betancourt Luis, Hernández Luis, Rada Pedro
Laboratory of Behavioral Physiology, School of Medicine, University of Los Andes, Mérida, 5101-A, Venezuela.
Laboratory of Behavioral Physiology, School of Medicine, University of Los Andes, Mérida, 5101-A, Venezuela.
Neurosci Lett. 2017 Mar 6;642:158-162. doi: 10.1016/j.neulet.2017.02.014. Epub 2017 Feb 8.
The ketogenic diet (KD) is acknowledged as an unconventional option in the treatment of epilepsy. Several lines of investigation point to a possible role of glutamate and gamma-aminobutyric acid (GABA) as main contributors in this protective effect. Other biomolecules could also be involved in the beneficial consequence of the KD, for example, the diamine agmatine has been suggested to block imidazole and glutamate NMDA receptor and serves as an endogenous anticonvulsant in different animal models of epilepsy. In the present report, we have used microdialysis coupled to capillary electrophoresis to monitor microdialysate levels of GABA, glutamate and agmatine in the hippocampus of rats submitted to a KD for 15days compared to rats on a normal rat chow diet. A significant increase in GABA and agmatine levels while no change in glutamate levels was observed. These results support the notion that the KD modifies different transmitters favoring inhibitory over excitatory neurotransmitters.
生酮饮食（KD）被认为是治疗癫痫的一种非常规选择。多项研究表明，谷氨酸和γ-氨基丁酸（GABA）可能是这种保护作用的主要贡献者。其他生物分子也可能参与了生酮饮食的有益作用，例如，已有人提出二胺胍丁胺可阻断咪唑和谷氨酸NMDA受体，并在不同的癫痫动物模型中作为内源性抗惊厥剂。在本报告中，我们使用微透析结合毛细管电泳来监测与正常大鼠饲料喂养的大鼠相比，接受15天KD的大鼠海马中GABA、谷氨酸和胍丁胺的微透析液水平。结果观察到GABA和胍丁胺水平显著升高，而谷氨酸水平没有变化。这些结果支持了生酮饮食改变不同递质，有利于抑制性神经递质而非兴奋性神经递质的观点。
