Electrically-evoked dopamine and acetylcholine release from rat striatal slices perfused without magnesium: regulation by glutamate acting on NMDA receptors.

1. Rat striatal slices, preincubated with [3H]-dopamine and [14C]-choline, were continuously superfused and electrically stimulated. Electrically evoked release of [3H]-dopamine and [14C]-acetylcholine (ACh) was not significantly changed by elimination of Mg2+ from superfusion buffer, but the basal release of [3H]-dopamine was doubled. 2. Kynurenic acid (100-800 microM) caused, in the absence but not presence of Mg2+, a concentration-dependent decrease in the evoked release of these two transmitters. The addition of glycine reversed the inhibition of the evoked release of both transmitters caused by kynurenic acid (400 microM) in a concentration-dependent manner. In addition, glycine increased the evoked release of [3H]-dopamine via a site inhibitable by strychnine (1 microM). 3. Another two antagonists at N-methyl-D-aspartate (NMDA) receptors, 2-amino-5-phosphonovaleric acid and dizocilpine, also decreased significantly the evoked release of the two transmitters in a concentration-dependent manner in the absence, but not presence of Mg2+. By contrast, an antagonist of non-NMDA receptors, 6-cyano-7-nitroquinoxaline-2,3-dione (10 microM) significantly decreased the evoked release of the two transmitters in the presence, but not in the absence of Mg2+. 4. Electrical field stimulation evoked release of endogenous adenosine, and this release tended to be higher in the absence of Mg2+. However, the addition of a selective adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (200 nM) did not influence the evoked release of the two transmitters, showing that the released adenosine is of little importance in controlling ACh and dopamine release from striatal slices. Non-NMDA receptors may play a similar role when Mg2+ ions are present. 5. The results indicate that NMDA receptors activated in the absence of Mg2+ participate in the electrically-evoked release of [3H]-dopamine and [14C]-ACh from the striatum.