摘要
目的从神经递质方面研究褪黑素(melatonin,Mel)抗癫痫作用的生化机制。方法采用匹罗卡品(pilocarpine,PILO)诱发大鼠癫痫持续状态(status epilepticus,SE)模型,观察大鼠SE后4个时相点即6、48、72h和7 d海马γ-氨基丁酸、谷氨酸含量和谷氨酸脱羧酶、γ-氨基丁酸转氨酶活性的变化,以及Mel对其变化的影响。结果PILO诱导大鼠SE后6 h^7 d海马谷氨酸含量显著升高,γ-氨基丁酸含量和谷氨酸脱羧酶活性显著降低,与对照组比较差异有统计学意义(P<0.05),γ-氨基丁酸转氨酶活性在SE后72 h才显著下降(P<0.05);给予Mel的大鼠在SE后6 h^7 d,海马γ-氨基丁酸含量和谷氨酸脱羧酶活性均显著高于仅予PILO处理的大鼠(P<0.05),而谷氨酸含量和γ-氨基丁酸转氨酶活性与仅予PILO处理的大鼠比较差异无统计学意义(P>0.05)。结论Mel通过增强SE大鼠海马谷氨酸脱羧酶活性及γ-氨基丁酸合成发挥抗癫痫作用。
Objective To study the biochemical mechanisms of melatonin as anticonvulsant from the neurotransmitter point of view. Methods Model of status epilepticus （SE） was induced by pilocarpine; Observing the changes of γ-aminobutyric acid （GABA）, glutamic acid （Glu） content and glutamic acid decarboxylase （GAD）, γ-aminobutyric acid-transaminase（GABA-T） activity at 6 h, 48 h, 72 h, and 7 d in hippocampus of rats after SE was induced. And to observe the effect of melatonin on these changes. Results The level of GABA and GAD activity was significantly lower and the level of Glu was significantly higher in hippocampus post-SE in pilocarpine group than the control （P〈0.05）. GABA-T activity was significantly decreased just at 72 h post-SE （P〈0.05）; At 6 h～7 d post-SE, the GABA content and GAD activity in hippocampus was significantly higher in rats treated with both pilocarpine and melatonin than that in rats only treated with pilocarpine （P〈0.05）. There was no significant difference of Glu content and GABA-T activity between pilocarpine treated group and both pilocarpine and melatonin treated group （P〉0.05）. Conclusions The anticonvulsive effect of melatonin may be due to increasing GAD activity and GABA content.
出处
《中国神经免疫学和神经病学杂志》
CAS
2006年第5期303-306,共4页
Chinese Journal of Neuroimmunology and Neurology
关键词
癫痫持续状态
海马
褪黑素
γ-氨基丁酸
status epilepticus
hippocampus
melatonin
γ-aminobutyric acid
