Dopamine release in the nucleus caudatus and in the nucleus accumbens is under glutamatergic control through non-NMDA receptors: a study in freely-moving rats.

Perfusion with quisqualate (5 x 10(-6) M) and kainate (5 x 10(-7) M), selective agonists of glutamate receptors, enhanced the release of dopamine in both caudate and accumbens nuclei of freely-moving rats, measured by the transcerebral microdialysis technique. In contrast, N-methyl-D-aspartate (NMDA) did not affect dopamine release, except at very high concentrations (10(-2) M). The quisqualate-kainate antagonist, FG 9041 (DNQX), antagonized the elevation of dopamine release induced by quisqualate and, furthermore, reduced that of kainate. CPP, a selective NMDA antagonist, did not counteract the quisqualate- or kainate-induced stimulation of dopamine release. The enhancement of dopamine release after quisqualate and kainate was accompanied by behavioural stimulation characterized by grooming, rearing, hypermotility with sniffing and confined sniffing. This behavioural syndrome could be blocked by haloperidol. Conversely, perfusion with NMDA did not activate behaviour even at high concentrations. These results indicate that the dopaminergic system, within the caudate and the accumbens nuclei, is under glutamatergic control through kainate and quisqualate receptors, while the NMDA receptors do not appear to be involved.