Role of nitric oxide in modulating the release of dopamine, glutamate, and GABA in striatum of the freely moving rat.

This study investigated the role of nitric oxide (NO) in modulating the basal and N-methyl-D-aspartate (NMDA)-induced release of dopamine (DA), glutamate (GLU), and gamma-aminobutiric acid (GABA) in striatum of the freely moving rat using microdialysis. Intrastriatal infusion of NMDA (5 mM) for 15 min increased extracellular concentrations of DA, GLU, and GABA. NMDA also decreased extracellular concentrations of DA metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC), and 4-hydroxy-3-methoxyphenylacetic acid (HVA), and of the GLU and GABA precursor, glutamine (GLN). Perfusion of N-nitroarginine (1-5 mM), an inhibitor of the synthesis of NO, potentiated NMDA-induced increases in extracellular concentrations of DA and attenuated increases of extracellular GLU. NMDA-induced decreases of extracellular concentrations of DOPAC were also attenuated by N-nitroarginine. N-nitroarginine had no effect on NMDA-induced changes of extracellular concentrations of GABA, HVA, and GLN. N-nitroarginine decreased basal concentrations of DOPAC and HVA, and increase basal concentrations of GLN, but had no effect on basal DA, GLU, and GABA. These results suggest a role for NO in modulating the NMDA-induced release of DA and GLU in striatum. They also suggest that NO could be regulating the basal metabolism of DA, GLU, and GABA.