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

• Published in: Cell research Vol. 11; no. 1; pp. 61 - 67
• Main Authors: Ma, Ying Hua, Hu, Jia Hua, Zhao, Wen Juan, Fei, Jian, Yu, Yun, Zhou, Xiao Gang, Mei, Zhen Tong, Guo, Li He
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group 01.03.2001
• ISSN: 1001-0602; 1748-7838
• DOI: 10.1038/sj.cr.7290067

Gamma-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 GABA(A) 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.