Compensatory Mechanisms Modulate the Neuronal Excitability in a Kainic Acid-Induced Epilepsy Mouse Model

Gaojie Pan, Zhicai Chen, Honghua Zheng, Yunwu Zhang, Huaxi Xu, Guojun Bu, Hui Zheng, Yanfang Li

Research output: Contribution to journalArticlepeer-review

4 Scopus citations


Epilepsy is one of the most common neurological disorders affecting millions of people. Due to the complicated and unclear mechanisms of epilepsy, still a significant proportion of epilepsy patients remain poorly controlled. Epilepsy is characterized by convulsive seizures that are caused by increased excitability. In this study, by using kainic acid (KA)-induced epilepsy mice, we investigated the neuronal activities and revealed the neuronal compensatory mechanisms after KA-induced toxic hyperexcitability. The results indicate that both phasic inhibition induced by enhanced inhibitory synaptic activity and tonic inhibition mediated by activated astrocytes participate in the compensatory mechanisms. Compensatory mechanisms were already found in various neuronal disorders and were considered important in protecting nervous system from toxic hyperexcitability. This study hopefully will provide valuable clues in understanding the complex neuronal mechanisms of epilepsy, and exploring potential clinical treatment of the disease.

Original languageEnglish (US)
Article number48
JournalFrontiers in Neural Circuits
StatePublished - Jun 29 2018


  • Epilepsy
  • Hyperexcitability
  • Kainic acid
  • Synaptic transmission
  • Tonic inhibition
  • γ-aminobutyric acid

ASJC Scopus subject areas

  • Neuroscience (miscellaneous)
  • Sensory Systems
  • Cognitive Neuroscience
  • Cellular and Molecular Neuroscience


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