Effects of anti-epileptic drugs on spreading depolarization-induced epileptiform activity in mouse hippocampal slices

被引：0
作者：
Ching-Huei Lin
Shih-Pin Hsu
Ting-Chun Cheng
Chin-Wei Huang
Yao-Chang Chiang
I-Han Hsiao
Ming-Hsueh Lee
Mei-Lin Shen
Dong Chuan Wu
Ning Zhou
机构：
[1] Graduate Institute of Biomedical Sciences,Department of Neurology
[2] China Medical University,Department of Neurology
[3] Translational Medicine Research Center,Department of Nursing
[4] China Medical University Hospital,Department of Neurosurgery
[5] E-DA Hospital,undefined
[6] I-Shou University,undefined
[7] National Cheng Kung University Hospital,undefined
[8] College of Medicine,undefined
[9] National Cheng Kung University,undefined
[10] Center for Drug Abuse and Addiction,undefined
[11] China Medical University Hospital,undefined
[12] China Medical University,undefined
[13] Division of Basic Medical Sciences,undefined
[14] Chang Gung University of Science and Technology,undefined
[15] China Medical University Hospital,undefined
[16] Division of Neurosurgery,undefined
[17] Department of Surgery,undefined
[18] Chang Gung Memorial Hospital,undefined
来源：
Scientific Reports | / 7卷
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摘要：
Epilepsy and spreading depolarization (SD) are both episodic brain disorders and often exist together in the same individual. In CA1 pyramidal neurons of mouse hippocampal slices, induction of SD evoked epileptiform activities, including the ictal-like bursts, which occurred during the repolarizing phase of SD, and the subsequent generation of paroxysmal depolarization shifts (PDSs), which are characterized by mild depolarization plateau with overriding spikes. The duration of the ictal-like activity was correlated with both the recovery time and the depolarization potential of SD, whereas the parameters of PDSs were not significantly correlated with the parameters of SD. Moreover, we systematically evaluated the effects of multiple anti-epileptic drugs (AEDs) on SD-induced epileptiform activity. Among the drugs that are known to inhibit voltage-gated sodium channels, carbamazepine, phenytoin, valproate, lamotrigine, and zonisamide reduced the frequency of PDSs and the overriding firing bursts in 20–25 min after the induction of SD. The GABA uptake inhibitor tiagabine exhibited moderate effects and partially limited the incidence of PDSs after SD. AEDs including gabapentin, levetiracetam, ethosuximide, felbamate, and vigabatrin, had no significant effect on SD-induced epileptic activity. Taken together, these results demonstrate the effects of AEDs on SD and the related epileptiform activity at the cellular level.
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