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大鼠脑内 kainic 酸诱导癫痫发作后质子磁共振波谱代谢物的时间变化。

Temporal changes in proton MRS metabolites after kainic acid-induced seizures in rat brain.

作者信息

Najm I M, Wang Y, Hong S C, Lüders H O, Ng T C, Comair Y G

机构信息

Department of Neurology, Cleveland Clinic Foundation, Ohio 44195, USA.

出版信息

Epilepsia. 1997 Jan;38(1):87-94. doi: 10.1111/j.1528-1157.1997.tb01082.x.

DOI:10.1111/j.1528-1157.1997.tb01082.x
PMID:9024189
Abstract

PURPOSE

In situ 1H-magnetic resonance spectroscopy (MRS) was used to study temporal metabolic changes in a rat model of temporal lobe epilepsy (TLE) by using kainic acid (KA).

METHODS

Rat brains were scanned at the level of the hippocampal body for MRS measurements. Relative ratios of N-acetyl groups (NA: N-acetylaspartate and N-acetylaspartyl glutamate), choline, and lactate (Lac) over creatine (Cr) were calculated.

RESULTS

NA/Cr ratios increased significantly during the ictal phase. During the postictal and interictal phases, the NA/Cr ratio decreased. There was a significant and prolonged increase of the lactate/Cr ratio in the hippocampi of rats that started 1 h after the onset of KA-induced seizure activity and persisted up to 24 h after the injection. The prolonged lactate/Cr increase in an area susceptible to neuronal damage (e.g., hippocampus) correlated with the onset of seizure activity but remained elevated thereafter.

CONCLUSIONS

The ictal and early postictal increase in lactate ratios may reflect increased cellular activity and metabolism resulting from KA excitotoxicity. Assuming that the changes in NA/Cr ratios are due to NAA increase, we speculate that an activation of the N-acetylaspartylglutamate (NAAG) dipeptidase pathway may explain the ictal increase in NA/Cr ratios. The late postictal decrease in NA/Cr ratios is a reflection of KA-induced neuronal cell loss.

摘要

目的

采用原位¹H磁共振波谱(MRS)技术,利用 kainic 酸(KA)研究颞叶癫痫(TLE)大鼠模型中的颞叶代谢变化。

方法

在海马体水平对大鼠脑进行扫描以进行 MRS 测量。计算 N - 乙酰基(NA:N - 乙酰天门冬氨酸和 N - 乙酰天门冬氨酰谷氨酸)、胆碱和乳酸(Lac)与肌酸(Cr)的相对比值。

结果

发作期 NA/Cr 比值显著升高。发作后期和发作间期,NA/Cr 比值下降。在 KA 诱导的癫痫发作活动开始后 1 小时开始,大鼠海马体中乳酸/肌酸比值显著且持续升高,并在注射后持续长达 24 小时。在易受神经元损伤的区域(如海马体)中乳酸/肌酸比值的持续升高与癫痫发作活动的开始相关,但此后仍保持升高。

结论

发作期和发作早期乳酸比值升高可能反映了 KA 兴奋性毒性导致的细胞活性和代谢增加。假设 NA/Cr 比值的变化是由于 NAA 增加,我们推测 N - 乙酰天门冬氨酰谷氨酸(NAAG)二肽酶途径的激活可能解释了发作期 NA/Cr 比值的升高。发作后期 NA/Cr 比值下降反映了 KA 诱导的神经元细胞丢失。

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