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癫痫发作及癫痫诱导神经元损伤的磁共振波谱代谢标志物。

MRS metabolic markers of seizures and seizure-induced neuronal damage.

作者信息

Najm I M, Wang Y, Shedid D, Lüders H O, Ng T C, Comair Y G

机构信息

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

出版信息

Epilepsia. 1998 Mar;39(3):244-50. doi: 10.1111/j.1528-1157.1998.tb01368.x.

Abstract

PURPOSE

Proton magnetic resonance spectroscopy (MRS) was used to identify specific in situ metabolic markers for seizures and seizure-induced neuronal damage. Kainic acid (KA)-induced seizures lead to histopathologic changes in rat brain. The protective effect of cycloheximide treatment against neuronal damage caused by KA-induced seizures was studied, using in situ proton MRS imaging technique.

METHODS

Rats were pretreated with placebo or cycloheximide 1 h before KA injection. Rat brains (n = 25) were scanned at the level of the hippocampus before, during, and 24 h after seizures. Spectra were recorded and the relative ratios of N-acetylaspartate (NAA), choline (cho), and lactate (Lac) to creatine (Cr) were calculated and compared between groups.

RESULTS

A significant increase in Lac ratios was observed in KA-treated rats during and 24 h after seizure onset and this increase was prevented by cycloheximide pretreatment. NAA ratios were significantly higher during the ictal phase following KA treatment and this effect was not affected by cycloheximide pretreatment. Nissl staining confirmed previously reported prevention of KA-induced neuronal loss in CA3 and CA1 areas of the hippocampus by cycloheximide pretreatment.

CONCLUSIONS

Our results suggest that in situ Lac increase is a marker of seizure-induced neuronal damage, whereas N-acetylaspartate (NAA) changes during and after status epilepticus may be a reflection of neuronal activity and damage, respectively.

摘要

目的

采用质子磁共振波谱(MRS)技术识别癫痫发作及癫痫发作诱导的神经元损伤的特异性原位代谢标志物。海藻酸(KA)诱导的癫痫发作会导致大鼠脑内出现组织病理学变化。本研究利用原位质子MRS成像技术,探讨放线菌酮治疗对KA诱导的癫痫发作所致神经元损伤的保护作用。

方法

在注射KA前1小时,对大鼠进行安慰剂或放线菌酮预处理。在癫痫发作前、发作期间及发作后24小时,对25只大鼠的脑在海马水平进行扫描。记录波谱,并计算N-乙酰天门冬氨酸(NAA)、胆碱(cho)、乳酸(Lac)与肌酸(Cr)的相对比值,比较组间差异。

结果

在KA处理的大鼠中,癫痫发作开始时及发作后24小时观察到Lac比值显著升高,而放线菌酮预处理可防止这种升高。KA处理后发作期NAA比值显著升高,且该效应不受放线菌酮预处理的影响。尼氏染色证实了先前报道的放线菌酮预处理可预防KA诱导的海马CA3和CA1区神经元丢失。

结论

我们的结果表明,原位Lac升高是癫痫发作诱导的神经元损伤的标志物,而癫痫持续状态期间及之后N-乙酰天门冬氨酸(NAA)的变化可能分别反映了神经元活动和损伤。

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