Deficit of quantal release of GABA in experimental models of temporal lobe epilepsy
Deficit of quantal release of GABA in experimental models of temporal lobe epilepsy
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DOI：
10.1038/9142
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发表时间：
1999-06-01
影响因子：
25
通讯作者：
Bernard, C
中科院分区：
文献类型：
--
作者：
Hirsch, JC;Agassandian, C;Bernard, C
由于GABA（γ-氨基丁酸）受体介导的抑制控制着大脑中主要神经元的兴奋性，因此GABA能抑制的缺陷一直被认为是癫痫发作的原因。在颞叶癫痫的实验模型中，我们已经确定了突触前GABA能末梢的抑制缺陷，其特征在于与突触囊泡密度降低相关的GABA量子活性降低。这种囊泡数量的减少似乎主要影响储备池，而不是停靠或容易释放的池。
Because GABA (γ-aminobutyric acid) receptor-mediated inhibition controls the excitability of principal neurons in the brain, deficits in GABAergic inhibition have long been favored to explain seizures. In an experimental model of temporal lobe epilepsy, we have identified a deficit of inhibition in presynaptic GABAergic terminals characterized by decreased GABA quantal activity associated with reduced synaptic vesicle density. This decrease in vesicle number primarily seems to affect the reserve pool, rather than the docked or the readily releasable pool.