Abstract #0950

Patel A, Behar K, Rothman D, de Graaf R

The purpose of the present study was to assess the potential contribution of the GABA reuptake pathway to total GABA release. Cerebral metabolic rates were measured in halothane anesthetized rats using in vivo 1H-[13C]-NMR in conjunction with intravenous [1,6-13C2]glucose infusion under conditions in which the primary neuronal GABA transporter (GAT-1) was blocked by tiagabine. Glutamatergic and GABAergic neurotransmission is decreased slightly following tiagabine treatment suggesting a high degree of coupling, possibly due to reduced glutamatergic activity of the elevated extracellular GABA expected with tiagabine treatment. We conclude that the contribution of neuronal reuptake to synaptically released GABA is less than previously expected.