GABA changes with vigabatrin in the developing human brain.

GABA changes with vigabatrin in the developing human brain.
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GABA 在人类大脑发育过程中随氨己烯酸发生变化。

DOI:
10.1111/j.1528-1157.1999.tb00741.x
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发表时间:
1999
期刊:
影响因子:
5.6
通讯作者:
Rothman,DL
Rothman,DL
中科院分区:
医学1区
文献类型:
--
作者:
NovotnyJr,EJ;Hyder,F;Shevell,M;Rothman,DL

文献摘要

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目的:γ-氨基丁酸(GABA)生理学的变化在确定发育中的神经系统的癫痫易感性方面很重要。非侵入性测量脑GABA在成人癫痫发作控制,脑GABA水平,脑GABA的变化与药物设计改变GABA代谢之间的重要关系。本研究的目的是证明GABA在枕叶癫痫儿童治疗后的氨己烯酸(VGB)。方法:10质子核磁共振波谱(NMRS)研究获得了4例癫痫患者。受试者年龄在1至5岁之间。结果:VGB治疗后,脑内GABA含量明显升高(P < 0.05,配对t检验)。在一个主题中,大脑GABA减少的癫痫灶的区域相比,对侧半球的同源区域。在VGB治疗后,在这个subject.Conclusions:VGB增加脑GABA水平的癫痫儿童在癫痫区域发生了近五倍的GABA增加。NMRS可用于监测大脑GABA水平对已知改变GABA生理学的药物的反应,并作为了解GABA介导的抑制在儿科癫痫中的作用的重要工具。
Purpose:Changes in γ‐aminobutyric acid (GABA) physiology are important in determining seizure susceptibility in the developing nervous system. Noninvasive measurements of brain GABA in adults with epilepsy have demonstrated important relations among seizure control, brain GABA levels, and changes in brain GABA with drugs designed to alter GABA metabolism. The purpose of this study was to demonstrate the changes in GABA in the occipital lobes of children with epilepsy after treatment with vigabatrin (VGB).Methods:Ten proton nuclear magnetic resonance spectroscopic (NMRS) studies were obtained on four subjects with epilepsy. The subjects were between ages 1 and 5 years. Occipital lobe GABA levels were measured before and after treatment with VGB.Results:Brain GABA levels increased significantly in these subjects after VGB treatment (p < 0.05, paired Student'sttest). In one subject, brain GABA was decreased in the region of the epileptic focus compared with the homologous region of the opposite hemisphere. A nearly fivefold increase in GABA occurred in the epileptic region after VGB treatment in this subject.Conclusions:VGB increases brain GABA levels in children with epilepsy. NMRS can be used to monitor the response of brain GABA levels to drugs known to alter GABA physiology and serve as an important tool to understand the role of GABA‐mediated inhibition in pediatric epilepsies.