Glutamate stimulates dopamine release from cortical and limbic rat brain in vitro

In vitro superfusion studies were performed to compare the glutamatergic control of dopamine release from minislices of rat striatum, olfactory tubercle and frontal cortex. In the absence of Mg2+, release of endogenous dopamine from olfactory tubercle and striatum, and [3H]dopamine from frontal cortex, was stimulated by glutamate (at concentrations of 0.3, 3 and 1 mM respectively). In all three areas the response to N-methyl-D-aspartate (NMDA) was greater than that to kainate, implying mediation largely by NMDA receptors, with non-NMDA receptors contributing to a smaller extent. This was confirmed by antagonist studies in the frontal cortex, where the response to glutamate was largely (70%) blocked by 2-amino-5-phosphonopentanoic acid (AP5), and further blocked by AP5 + 6,7-dinitroquinoxaline-2,3-dione (DNQX). In the olfactory tubercle and striatum, glutamate was as effective as NMDA, but in the frontal cortex the response to NMDA was significantly larger than that to glutamate.