ELECTRICALLY-EVOKED DOPAMINE AND ACETYLCHOLINE-RELEASE FROM RAT STRIATAL SLICES PERFUSED WITHOUT MAGNESIUM - REGULATION BY GLUTAMATE ACTINGON NMDA RECEPTORS

1 Rat striatal slices, preincubated with [H-3]-dopamine and [C-14]-cho line, were continuously superfused and electrically stimulated. Electr ically evoked release of [H-3]-dopamine and [C-14]-acetylcholine (ACh) was not significantly changed by elimination of Mg2+ from superfusion buffer, but the basal release of [H-3]-dopamine was doubled. 2 Kynure nic acid (100-800 mu M) caused, in the absence but not presence of Mg2 +, a concentration-dependent decrease in the evoked release of these t wo transmitters. The addition of glycine reversed the inhibition of th e evoked release of both transmitters caused by kynurenic acid (400 mu M) in a concentration-dependent manner. In addition, glycine increase d the evoked release of [H-3]-dopamine via a site inhibitable by stryc hnine (1 mu M). 3 Another two antagonists at N-methyl-D-aspartate (NMD A) receptors, 2-amino-5-phosphonovaleric acid and dizocilpine, also de creased 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-nitroqui noxaline-2,3-dione (10 mu M) significantly decreased the evoked releas e of the two transmitters in the presence, but not in the absence of M g2+. 4 Electrical field stimulation evoked release of endogenous adeno sine, and this release tended to be higher in the absence of Mg2+. How ever, the addition of a selective adenosine A(1) receptor antagonist 8 -cyclopentyl-1,3-dipropylxanthine (200 nM) did not influence the evoke d 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 Mg2ions are present. 5 The results indicate that NMDA receptors activated in the absence of Mg2+ participate in the electrically-evoked release of [H-3]-dopamine and [C-14]-ACh from the striatum.