Abstract
Using microdialysis, the effects of endogenous dopamine on basal extracellular concentrations of γ-aminobutyric acid (GABA) and on the increases of GABA produced by glutamate were investigated in the medial prefrontal cortex of the awake rat. The dopamine uptake inhibitor nomifensine (1, 100 and 1000 μM), used to increase extracellular dopamine, produced a dose-related increase of dialysate dopamine (0.1–1 nM) but did not change dialysate concentrations of GABA or glutamate at any dose used. The glutamate uptake inhibitor L- trans-pyrrolidine-2,4-dicarboxilic acid (PDC; 0.5 and 2 mM), used to increase extracellular glutamate, produced a dose-related increase of dialysate glutamate (1.5–5.5 μM) and increased dialysate GABA by 125%. When a simultaneous increase of endogenous dopamine and glutamate was produced, the increases of dialysate GABA were significantly higher (185% of baseline) than those produced by glutamate alone. These effects on dialysate GABA were attenuated by the D2 receptor antagonist (−) sulpiride, but not by the D1 receptor antagonist SCH-23390, all of which suggests that extracellular dopamine plays an important role in modulating endogenous glutamate-GABA interactions in the prefrontal cortex of the rat.
Published Version
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