The utility of glial molecular imaging in epileptic animal brain.

锂-匹罗卡品（Li-P）诱导大鼠脑神经胶质细胞能量代谢明显增强。神经胶质代谢用^<14> c -乙酸测定。在成年（8周龄）大鼠脑中观察到脑摄取增加。在癫痫持续状态（SE）期间，幼龄（3周龄）大鼠脑中的c -乙酸摄取没有改变，而在SE期间，幼龄大鼠脑中的局部脑血流量和葡萄糖代谢均有所增加。丙酮的抗惊厥作用已在各种癫痫动物模型中得到报道。我们还证实了酮体甲基乙基酮（MEK）和二乙基酮（DEK）对Li-P诱导的SE有抑制作用。MEK和DEK在化学和电休克诱导的实验癫痫模型中均表现出广谱抗惊厥作用。

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.