Abstract

In vivo intracerebral microdialysis studies with high-performance liquid chromatography and electrochemical detection in Sprague–Dawley rats showed that administration of the dopamine D2 receptor antagonist raclopride (20 and 100 μM) into the nucleus accumbens did not alter the baseline extracellular citrulline level (a co-product of NO synthesis) in the nucleus accumbens. Administration of NMDA (100 μM), an NMDA glutamate receptor agonist, into the nucleus accumbens induced an increase in the extracellular citrulline level in this structure. Administration of 7-nitroindazole (0.5 mM), an inhibitor of the neuronal isoform of NO synthase, into the nucleus accumbens blocked this increase, while administration of raclopride (20 and 100 μM) into this structure decreased the increase. These data suggest that dopamine D2 receptors in the nucleus accumbens are involved in regulation of the extent of activation of neuronal NO synthase induced by local stimulation of NMDA glutamate receptors.

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