Overexpression of γ-aminobutyric acid transporter subtype I leads to susceptibility to kainic acid-induced seizure in transgenic mice

Yinghua Ma, Jia Hua Hu, Wen Juan Zhao, Jian Fei, Yun Yu, Xiao Gang Zhou, Zhen Tong Mei, Li He Guo

Research output: Contribution to journalArticlepeer-review

Abstract

γ-aminobutyric acid (GABA) is the principal inhibitory neurotransmitter, and the GABAergic synaptic transmission is normally terminated by the rapid uptake through GABA transporters. With transgenic mice ubiquitously overexpressing GABA transporter subtype I (GAT1), the present study explored the pathophysiological role of GAT1 in epileptogenesis. Though displaying no spontaneous seizure activity, these mice exhibit altered electroencephalographic patterns and increased susceptibility to seizure induced by kainic acid. In addition, the GABAA receptor and glutamate transporters are up-regulated in transgenic mice, which perhaps reflects a compensatory or corrective change to the elevated level of GAT1. These preliminary findings support the hypothesis that excitatory and inhibitory neurotransmission, and seizure susceptibility can be altered by neurotransmitter transporters.

Original languageEnglish (US)
Pages (from-to)61-67
Number of pages7
JournalCell Research
Volume11
Issue number1
DOIs
StatePublished - Mar 2001

Keywords

  • Electroencephalography
  • Kainic acid
  • Seizure
  • Susceptibility
  • Transgenic mice
  • γ-aminobutyric acid transporter

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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