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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 >Dietary supplementation with acetyl-l-carnitine in seizure treatment of pentylenetetrazole kindled mice
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Dietary supplementation with acetyl-l-carnitine in seizure treatment of pentylenetetrazole kindled mice

机译：膳食补充乙酰基左旋肉碱治疗癫痫发作的戊四氮点燃的小鼠

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In spite of the availability of new antiepileptic drugs a considerable number of epilepsy patients still have pharmacoresistant seizures, and thus there is a need for novel approaches. Acetyl-l-carnitine (ALCAR), which delivers acetyl units to mitochondria for acetyl-CoA production, has been shown to improve brain energy homeostasis and protects against various neurotoxic insults. To our knowledge, this is the first study of ALCAR's effect on metabolism in pentylenetetrazole (PTZ) kindled mice. ALCAR or the commonly used antiepileptic drug valproate, was added to the drinking water of mice for 25 days, and animals were injected with PTZ or saline three times a week during the last 21 days. In order to investigate ALCAR's effects on glucose metabolism, mice were injected with [1- 13C]glucose 15 min prior to microwave fixation. Brain extracts from cortex and the hippocampal formation (HF) were studied using 1H and 13C NMR spectroscopy and HPLC. PTZ kindling caused glucose hypometabolism, evidenced by a reduction in both glycolysis and TCA cycle turnover in both brain regions investigated. Glutamatergic and GABAergic neurons were affected in cortex and HF, but the amount of glutamate was only reduced in HF. Slight astrocytic involvement could be detected in the cortex. Interestingly, the dopamine content was increased in the HF. ALCAR attenuated the PTZ induced reduction in [3- 13C]alanine and the increase in dopamine in the HF. However, TCA cycle metabolism was not different from that seen in PTZ kindled animals. In conclusion, even though ALCAR did not delay the kindling process, it did show some promising ameliorative effects, worthy of further investigation.
机译：尽管可获得新的抗癫痫药，但是仍有相当多的癫痫患者仍患有药敏性癫痫发作，因此需要新颖的方法。乙酰基-1-肉碱（ALCAR）可以向线粒体传递乙酰基以产生乙酰辅酶A，它已被证明可以改善脑能量稳态，并能防止各种神经毒性损伤。据我们所知，这是首次研究ALCAR对戊四氮（PTZ）点燃的小鼠代谢的影响。将ALCAR或常用的抗癫痫药丙戊酸盐加到小鼠的饮用水中，持续25天，在过去的21天中，每周三次给动物注射PTZ或盐水。为了研究ALCAR对葡萄糖代谢的影响，在微波固定之前15分钟给小鼠注射[1-13C]葡萄糖。使用1H和13C NMR光谱法和HPLC研究了皮质和海马结构（HF）的脑提取物。 PTZ点燃引起葡萄糖代谢低下，这在所研究的两个大脑区域的糖酵解和TCA循环转换均减少了。谷氨酸能和GABA能神经元在皮质和HF中受到影响，但是谷氨酸的量仅在HF中减少。在皮质中可以检测到轻微的星形细胞累及。有趣的是，HF中的多巴胺含量增加了。 ALCAR减弱了PTZ诱导的[3-1-13C]丙氨酸减少和HF中多巴胺的增加。但是，TCA循环代谢与PTZ点燃的动物没有什么不同。总而言之，即使ALCAR并没有延迟点燃过程，但确实显示出一些有希望的改善效果，值得进一步研究。

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