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Neurosci Lett. 1997 Jul 11;230(1):21-4.

Inhibition of glutamate reuptake potentiates endogenous nitric oxide-facilitated dopamine efflux in the rat striatum: an in vivo microdialysis study.

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  • 1Cellular and Clinical Neurobiology Program, Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, MI 48201, USA.


The current study investigated the effects of the nitric oxide synthase (NOS) substrate, N(G)-hydroxy-L-arginine (H-ARG) and the selective glutamate (GLU) reuptake inhibitor (2S)-trans-pyrrolidine-2,4-dicarboxylic acid (PDC) on striatal dopamine (DA) and glutamate (GLU) efflux in vivo. Concentric microdialysis probes were stereotaxically implanted in the anterior-medial striatum of chloral hydrate-anesthetized rats. Intra-striatal infusion of PDC (200 microM) elevated extracellular (EC) DA and GLU levels concurrently over a 10 fraction collecting period without affecting EC asparagine levels. Infusion of H-ARG (200 microM) for six 20-min fractions, also significantly elevated EC DA levels. In the presence of PDC (200 microM), co-perfusion of H-ARG (200 microM) resulted in supra-additive increases in EC DA levels. The synergistic effect of PDC and H-ARG infusion on DA efflux was attenuated by co-infusion of the NOS inhibitor, 7-nitroindazole (100-200 microM). These results suggest that while both endogenous NO and GLU regulate striatal DA efflux via facilitatory influences, enhanced glutamatergic tone on striatal NOS-containing neurons may potentiate NO-synthesis and subsequently NO-induced DA efflux.

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