Role of presynaptic dopamine receptors in regulation of the glutamatergic neurotransmission in rat neostriatum

Abstract

In experiments with the use of a push-pull cannula and simultaneous recording of electrical activity at the site of perfusion, the release of L-[3H]glutamic acid from rat neostriatum induced by K+-depolarization (60 mM K+ in perfusate) has been shown to be inhibited by replacing Ca2+ in the perfusion medium by Co2+. In contrast, release of L-[3H]glutamate induced by electrical stimulation of frontal cortex is enhanced by replacement of these cations. Application of dopamine (10(-5)-10(-3) M). apomorphine (10(-4) M) or beta-phenylethylamine (10(-3) M) as well as stimulation of the substantia nigra enhanced the basal release of L-[3H]glutamate. Haloperidol (10(-4) M) completely abolished the effects of apomorphine and beta-phenylethylamine, and partially abolished the effect of dopamine. The enhancement induced by apomorphine is strongly dependent on the presence of Na+ in the perfusion medium. On the other hand, apomorphine (10(-4) M) and beta-phenylethylamine (10(-3) M) inhibited the release of glutamate induced by electrical stimulation of the frontal cortex and that by K+-depolarization (the latter was shown for apomorphine). This inhibition is also abolished by haloperidol. A possible functional role of endogenous dopamine in the regulation of glutamatergic neurotransmission in rat neostriatum is discussed.