A push-pull cannula supplied with artificial CSF was implanted in the
striatum of anaesthetized rats, and the basal extracellular DA and DOP
AC was assayed in the superfusates using HPLC and electrochemical dete
ction. Simultaneously, a carbon fibre electrode was implanted in close
proximity of the cannula and the evoked DA release was detected by di
fferential pulse amperometry during stimulation of the DA axons. Local
treatments with cadmium (100 mu M) blocked the evoked DA release (-90
%), but substantially increased the basal extracellular DA (+125%). Th
e effects of glutamate agonists NMDA (1 mM) and kainate (0.1 mM), know
n to increase basal extracellular DA were confirmed (+150% and +60% re
spectively). It was, however, simultaneously observed that the evoked
DA release was inhibited (-80% and -50%, respectively). Amphetamine (1
mu M) released DA (+150%) and produced also an increase (+100%) of th
e evoked DA release. These results, apparently conflicting, show that
the two mechanisms releasing dopamine (firing-dependent and not) can b
e directly and simutaneously observed. These two releasing processes a
ppear to be not strictly antagonist. They are also differently and ind
ependently modulated by calcium and by local influences such those con
veyed by glutamate.