The utility of glial molecular imaging in epileptic animal brain.

在锂-匹罗卡品（Li-P）致痫大鼠模型中，胶质细胞能量代谢明显增强。神经胶质代谢用13 <14>C-乙酸盐测量。在成年（8周龄）大鼠脑中观察到脑摄取增加。在<14>癫痫持续状态（SE）期间，年轻大鼠（3周龄）脑中的^C-乙酸摄取没有变化，而在SE期间，年轻大鼠脑中的局部脑血流量和葡萄糖代谢均增加。丙酮的抗惊厥作用已在各种癫痫动物模型中报道。我们还证明了酮体，甲基乙基酮（MEK）和二乙基酮（DEK），抑制由Li-P诱导的大鼠SE。MEK和DEK在化学和电休克诱导的实验性癫痫模型中均显示出广谱抗惊厥作用。

Glial energy metabolism in rat brain was markedly enhanced during a prolonged seizure induced by lithium-pilocarpine (Li-P) model. Glial metabolism was measured with ^<14>C-acetate. The increase of brain uptake was observed in adult (8 weeks old) rat brain. ^<14>C-acetate uptake in young (3 weeks old) rat brain was not changed during status epilepticus (SE), whereas both local cerebral blood flow and glucose metabolism were increased in young rat brain during SE. The anticonvulsant effects of acetone have been reported in various animal models of epilepsy. We also demonstrated that ketone bodies, methyl ethyl ketone (MEK) and diethyl ketone (DEK), suppressed SE that was induced by Li-P in rat. And MEK and DEK showed broad-spectra anticonvulsant effects in both chemically- and electroshock-induced experimental seizure models.