Tasker J G, Dudek F E
Mental Retardation Research Center, UCLA School of Medicine 90024.
Neurochem Res. 1991 Mar;16(3):251-62. doi: 10.1007/BF00966088.
Epileptogenic conditions come about from a disequilibrium between excitatory and inhibitory mechanisms, creating a state of neuronal hypersynchrony. From experimental studies in animal models of epilepsy it appears that several mechanisms, alone or in combination, could be responsible for this imbalance. An alteration of GABA-mediated inhibition has long been considered to be one of the most likely candidates. We review recent data on the synaptic physiology of GABA-mediated inhibition, with emphasis on GABAA and GABAB receptors and their conductances. We describe the integrative role of GABAergic local-circuit neurons in the normal control of recurrent excitation. We then discuss possible alterations in GABAA-mediated inhibition in two chronic animal models of epilepsy, the kindled rat and the kainate-treated rat. Finally, we review studies on GABA inhibition in human epileptic cortex resected for the treatment of intractable epilepsy.
致痫情况源于兴奋和抑制机制之间的失衡，从而产生神经元超同步状态。从癫痫动物模型的实验研究来看，似乎有几种机制单独或共同作用可能导致这种失衡。长期以来，GABA介导的抑制作用改变一直被认为是最有可能的原因之一。我们回顾了关于GABA介导抑制的突触生理学的最新数据，重点是GABAA和GABAB受体及其电导。我们描述了GABA能局部回路神经元在正常控制反复性兴奋中的整合作用。然后，我们讨论了两种慢性癫痫动物模型——点燃大鼠和海藻酸盐处理大鼠中GABAA介导抑制的可能改变。最后，我们回顾了对因治疗顽固性癫痫而切除的人类癫痫皮层中GABA抑制的研究。
