Abstract

Dual probe microdialysis was employed to characterize the origins of dialysate glutamate, aspartate and gamma-aminobutyric acid (GABA) in the medial prefrontal cortex (mPfc) and to investigate functional interactions between the mPfc and ventral tegmental area (VTA) in awake, freely moving rats. Perfusion with elevated potassium (K +; KCl, 100 mM, 20 min), low Ca 2+ (0.1 mM, 60 min) or tetrodotoxin (TTX, 10 μM, 100 min) was performed in the mPfc and dialysate levels of glutamate, aspartate and GABA were measured locally and in the VTA. Elevated K + in the mPfc rapidly increased dialysate glutamate and aspartate locally (+90±10 and +41±9% from basal, respectively) and in the VTA (+71±14 and +42±14%, respectively). MPfc GABA was also rapidly increased (+241±62%) while VTA GABA was not affected. Perfusion with low Ca 2+ in the mPfc decreased local glutamate, aspartate and GABA (−26±8; −35±7 and −45±8%, respectively) and decreased only GABA (−40±5%) in the VTA. Intra-mPfc TTX increased glutamate and aspartate locally (+82±23 and +54±27%, respectively) and in the VTA (+84±18 and +38±17%, respectively). In contrast, intra-mPfc TTX decreased local GABA (−33+6%) while VTA GABA levels were not affected. Taken together, these data confirm the influence of the mPfc upon the ipsilateral VTA and provide evidence for two neuronal pools which contribute to basal extracellular mPfc and VTA glutamate, aspartate and GABA levels, the first pool derived from Na +- and Ca 2+-dependent release and the second derived from voltage-dependent reuptake.

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