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 tile effects of successive excitatory inputs oil tile epileptic activity induced in the absence of inhibitions. Pai,ed-pulsc orthodromic and antidromic stimulations were used to test the changes in the evoked responses in tile hippocampus. Picrotoxin （PTX）, y-aminobutyric acid （GABA） type A （GABAA） receptor antagonist, was added to block the inhibitory synaptic transmission and to establish the epileptic model. Extracellular evoked population spike （PS） was recorded m the CA I region of the hippocampus. The results showed that the ap- plication 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 re- sponses. 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, tile neurons may ignore the excitatory inputs and intrinsically generate bursts during epileptic activity. The depolarization block could bc tile mechanisms underlying the PPD in the absence of GABAA inhibitions. Tile dislinct neuronal responses to stimulations during different epileptic stages may implicate the different an- tiepileptic effects of electrical stimulation.
