中文摘要：

禁止的 synaptic 传播的机能障碍能在神经原破坏在有刺激性、禁止的 synaptic 输入之间的平衡，从而导致癫痫的活动。纸的目的是在当抑制不在时导致的癫痫的活动调查连续有刺激性的输入的效果。对脉搏 orthodromic 和逆行的刺激被用来在马头鱼尾的怪兽在唤起的回答测试变化。Picrotoxin (PTX ) ， -aminobutyric 酸(伽马氨基丁酸) 类型 A (GABAA ) 受体对手，被增加堵住禁止的 synaptic 传播并且建立癫痫的模型。细胞外的唤起的人口尖铁(PS ) 在马头鱼尾的怪兽的 CA1 区域被记录。结果证明 PTX 的申请在 PS 振幅的对脉搏比率导致了一个 biphasic 变化。第二 PS (PS2 ) 的短潜伏增加以后被 PS2 消沉的再现跟随。这类消沉在 orthodromic 和逆行的对脉搏回答被观察，而 GABAergic PS2 消沉[叫的对脉搏消沉(PPD )] 在基线期间，记录仅仅出现在唤起 orthodromic 的回答。另外，在约 100 ms 的消沉持续时间与一个相对沉默时期在 PTX 的延长申请导致的自发的爆炸分泌物以内观察了一致。在结论，神经原可以忽略有刺激性的输入并且内在地在癫痫的活动期间产生爆炸。去极块能是当 GABAA 抑制不在时位于 PPD 下面的机制。对刺激的不同 neuronal 回答可以在不同癫痫的阶段期间含有电的刺激的不同镇癫痫剂效果。

英文摘要：

Dysfunction of inhibitory synaptic transmission can destroy the balance between excitatory and inhibitory synaptic inputs in neurons,thereby inducing epileptic activity.The aim of the paper is to investigate the effects of successive excitatory inputs on the epileptic activity induced in the absence of inhibitions.Paired-pulse orthodromic and antidromic stimulations were used to test the changes in the evoked responses in the hippocampus.Picrotoxin（PTX）,γ-aminobutyric acid（GABA） type A（GABA A） receptor antagonist,was added to block the inhibitory synaptic transmission and to establish the epileptic model.Extracellular evoked population spike（PS） was recorded in the CA1 region of the hippocampus.The results showed that the application of PTX induced a biphasic change in the paired-pulse ratio of PS amplitude.A short latency increase of the second PS（PS2） was later followed by a reappearance of PS2 depression.This type of depression was observed in both orthodromic and antidromic paired-pulse responses,whereas the GABAergic PS2 depression [called paired-pulse depression（PPD）] during baseline recordings only appeared in orthodromic-evoked responses.In addition,the depression duration at approximately 100 ms was consistent with a relative silent period observed within spontaneous burst discharges induced by prolonged application of PTX.In conclusion,the neurons may ignore the excitatory inputs and intrinsically generate bursts during epileptic activity.The depolarization block could be the mechanisms underlying the PPD in the absence of GABA A inhibitions.The distinct neuronal responses to stimulations during different epileptic stages may implicate the different antiepileptic effects of electrical stimulation.