The γ-aminobutyric acid (GABA) and glutamate are, respectively, major
inhibitory and excitatory neurotransmitters in the central nervous system (CNS)
and are essential to the visual processing. Studies show that glutamate induces
the release of GABA in the retina, but the mechanisms involved in this release
are not well elucidated. Previous work also showed that thiols compounds
regulate GABA release, but are not well defined the effects of compounds
containing sulfhydryl (-SH) on endogenous levels of this neurotransmitter in the
retina. In this context, glutathione (GSH) besides being the most important thiols
compounds, have demonstrated perform a neuromodulatory role in the release
of neurotransmitters. Thus, the objective of this study was to evaluate a
possible modulatory effect of GSH on the release of GABA mediated by
glutamate in the retina of chick embryo. For this study, we used as experimental
model, retinal tissue intact chick embryo, with seven or eight days of
development. In tests of release of GABA, the retinas were treated with GSH
(100 and 500 μM), glutamate (50 and 500 μM) and Buthionine Sulfoximine
(BSO), an inhibitor of glutathione synthesis, (50 μM) per 15 minutes, and GABA
levels released into the extracellular medium were quantified by High
Performance Liquid Chromatography (HPLC). For release experiments of thiols
compounds, the retinas were incubated with glutamate 100 μM (with or without
Na +) per 15 minutes, and their extracellular levels were determined by reaction
with DTNB and quantified by spectrophotometry (412 nm). The results show
that glutamate, as well as GSH, release GABA. Our data also show that BSO
attenuates the release of GABA promoted by glutamate. Furthermore, we
demonstrate that glutamate induces release of thiol compounds regardless of
sodium. Therefore, it is known that glutamate is able to release thiols and
GABA, among them, GSH is most abundant and responsible for also release
GABA. It is also known that once inhibited GSH synthesis by BSO, the release
of GABA induced by glutamate is attenuated. Then, it is suggested a possible
modulation of GSH in the release of GABA induced by glutamate in retina intact
chicken embryo.
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