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

Overview

MeSH Major

  • Brain
  • Carrier Proteins
  • Genetic Predisposition to Disease
  • Membrane Proteins
  • Membrane Transport Proteins
  • Neural Inhibition
  • Neurons
  • Organic Anion Transporters
  • Seizures
  • gamma-Aminobutyric Acid

abstract

  • 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.

publication date

  • March 2001

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed ID

  • 11305326

Additional Document Info

start page

  • 61

end page

  • 7

volume

  • 11

number

  • 1