Effect of vigabatrin on glutamate dehydrogenase in the hippocampus of seizure prone gerbils

Neurosci Lett. 2003 Apr 10;340(2):115-8. doi: 10.1016/s0304-3940(03)00072-7.

Abstract

Vigabatrin (VGB, gamma-vinyl-gamma-aminobutyric acid (GABA)), an irreversible inhibitor of GABA transaminase, increases regional inhibitory effects by elevating GABA concentration and reducing glutamate synthesis. In the present study, changes in glutamate dehydrogenase (GDH) activity and its immunoreactivity in the seizure prone gerbil hippocampus after treating VGB were investigated to identify the effect of VGB on energy and/or glutamate metabolism via GDH. In the VGB treated group, GDH immunoreactivity and its activity in the hippocampus were significantly decreased, as compared with those of controls. These findings suggest that VGB administration may suppress the development and spread of seizures not only by elevating the level of GABA, but also by affecting the glutamate signaling and energy metabolism in neurons.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Enzyme Inhibitors / pharmacology*
  • Enzyme Inhibitors / therapeutic use
  • Gerbillinae
  • Glutamate Dehydrogenase / antagonists & inhibitors*
  • Glutamate Dehydrogenase / metabolism
  • Hippocampus / drug effects*
  • Hippocampus / enzymology
  • Seizures / drug therapy
  • Seizures / enzymology*
  • Vigabatrin / pharmacology*
  • Vigabatrin / therapeutic use

Substances

  • Enzyme Inhibitors
  • Glutamate Dehydrogenase
  • Vigabatrin