HIPPOCAMPAL GABA TRANSPORTER FUNCTION IN TEMPORAL-LOBE EPILEPSY
HIPPOCAMPAL GABA TRANSPORTER FUNCTION IN TEMPORAL-LOBE EPILEPSY
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DOI：
10.1038/376174a0
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发表时间：
1995-07-13
期刊：
影响因子：
64.8
通讯作者：
SPENCER, DD
中科院分区：
文献类型：
--
作者：
DURING, MJ;RYDER, KM;SPENCER, DD
对人类颞叶癫痫的电生理学研究表明，海马GABA介导的抑制的丧失可能是神经元过度兴奋的基础（1-3）。然而，含有GABA（γ-氨基丁酸）的细胞被保留（4），并且GABA受体维持在存活的海马神经元中（5）。因此，GABA释放减少可能介导抑制的丧失。在这里，我们表明，在人脑中，钾刺激释放的GABA增加，谷氨酸诱导的，钙非依赖性释放的GABA显着减少，在致痫性campi，与对侧，非致痫性campi。大鼠体内谷氨酸诱导的GABA释放是转运体介导的。此外，在杏仁核点燃的大鼠中，一种人类癫痫模型，谷氨酸诱导的GABA释放减少与GABA转运体数量减少48%相关。这些数据表明，颞叶癫痫的特点是部分损失的谷氨酸刺激的GABA释放是继发于GABA转运体的数量减少。
ELECTROPHYSIOLOGICAL studies of human temporal-lobe epilepsy suggest that a loss of hippocampal GABA-mediated inhibition may underlie the neuronal hyperexcitability(1-3). However, GABA (gamma-aminobutyric acid)-containing cells are preserved(4) and GABA receptors are maintained in the surviving hippocampal neurons(5). Diminished GABA release may therefore mediate the loss of inhibition. Here we show that, in the human brain, potassium-stimulated release of GABA was increased, and glutamate-induced, calcium-independent release of GABA was markedly decreased, in epileptogenic hippocampi, in contrast with contralateral, non-epileptogenic hippocampi. The glutamate-induced GABA release in vivo was transporter-mediated in rats. Furthermore, in amygdala-kindled rats, a model for human epilepsy, a decease in glutamate-induced GABA release was associated with a 48% decrease in tbe number of GABA transporters. These data suggest that temporal-lobe epilepsy is characterized in part by a loss of glutamate-stimulated GABA release that is secondary to a reduction in the number of GABA transporters.