gamma-aminobutyric acid infusion in substantia nigra pars reticulata in rats inhibits ascorbate release in ipsilateral striatum

A relatively high level of extracellular ascorbate in the striatum, which i s known to modulate impulse flow in striatal neurons, originates primarily from glutamate-containing corticostriatal afferents. Increasing evidence su ggests that ascorbate release from these fibers is regulated by a multisyna ptic loop that includes gamma-aminobutyric acid (GABA) mechanisms in the su bstantia nigra. To assess the role that nigral GABA plays in striatal ascor bate release, extracellular ascorbate was monitored voltammetrically in the striatum during infusions of GABA into the substantia nigra pars reticulat a (SNr) of awake, unrestrained rats. Compared to vehicle infusions, intrani gral GABA lowered striatal ascorbate by >50%. In contrast, intranigral appl ication of picrotoxin, a GABA antagonist, had the opposite effect. Neither GABA nor picrotoxin altered striatal 3,4-dihydroxyphenylacetic acid (DOPAC) , a major dopamine metabolite. Collectively, these results indicate that in tranigral GABA exerts a tonic inhibitory influence on ascorbate release in the striatum. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.