Abstract #3049

Shen J, Yang J

Increased endogenous GABA concentration has been found to cause increased release of the inhibitory neurotransmitter GABA. Evidence exists in the literature that elevated brain GABA concentration also reduces glutamate release. In this study, accompanying an increase in endogenous GABA concentration caused by administration of the antiepileptic drug vigabatrin, a significant reduction was found in 13C-label incorporation into the predominantly neuronal [4-13C]glutamate from the glia-specific substrate [2-13C]acetate, providing further evidence for a negative modulation of glutamatergic activity by increased endogenous GABA concentration.