A push-pull cannula supplied with an artificial cerebrospinal fluid containing the tritiated precursor of dopamine, [3H]tyrosine, was implanted in the caudate nucleus of rats anesthetized with halothane. The extracellular dopamine and dihydroxyphenylacetic acid were measured in successive 20 min fractions (both in their tritiated and unlabeled form) and the ratio between the two forms calculated. Glutamate was added to the superfusing cerebrospinal fluid to investigate its role in the process of dopamine release. The release of dopamine and the efflux of dihydroxyphenylacetic acid were activated by a low concentration (10(-8) M) of glutamate. In contrast, a higher concentration (10(-4) M) of the amino acid reduced the release of dopamine. These results first confirmed the presence of a dual mechanism of control, by glutamate, of the dopamine release in the striatum depending on the extracellular concentration. Secondly, these treatments affected the dihydroxyphenylacetic acid amount and predominantly the tritiated form of dopamine, suggesting that the glutamate induces an important increase of the amine synthesis, in spite of a moderate effect on the release. The reversal of the inhibition by applications of tetrodotoxin (5 x 10(-7) M) and bicuculline (10(-4) M) confirmed that it was mediated by an indirect mechanism involving a GABAergic neurotransmission. In addition, the increase of the spontaneous dopamine release during bicuculline application suggested the existence of a tonic mechanism of inhibition of dopamine release in the striatum. This was confirmed by the fact that local xylocaine-induced anesthesia of the sensory motor cortex increased the spontaneous release of dopamine in the striatum.(ABSTRACT TRUNCATED AT 250 WORDS)