Development of rat brain uptake and calcium-dependent release of GABA.
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Biomedical subjects
Publications and source records attributed to D A Redburn.
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Synaptosomes treated with radioactive gamma-aminobutyric acid can be stimulated to release this substance. The release is maximal within 40 seconds after stimulation and is dependent on calcium. Magnesium and manganese ions, known to block stimulus-secretion coupling processes, depress calcium-dependent release. This release is specific to synaptosomes because microsomal or myelin fractions do not release accumulated gamma-aminobutyric acid. The data illustrate a simple in vitro system suitable for analysis of secretion of gamma-aminobutyric acid in brain and in addition describe several new aspects of uptake and secretion of this compound at brain nerve endings.
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Previous studies have indicated that gamma-aminobutyric acid (GABA) plays an important trophic role in the synapse formation between horizontal cells and photoreceptors in postnatal rabbit retina. However, the mechanism of the GABA effect has not been identified. Using fluo-3 Ca2+ imaging and confocal laser scanning microscopy we examined the effect of GABA on [Ca2+]i during postnatal retinal development. GABA (100 microM) evoked a fast and transient increase of [Ca2+]i in selected populations of freshly dissociated retinal cells from postnatal rabbits. This increase was apparent on postnatal day 1 and reached a maximum on day 5. Little increase in [Ca2+]i was observed in retinal cells isolated from adult rabbits. GABA receptor antagonists, picrotoxin and bicuculline, significantly reduced the response. The GABAB agonist, baclofen, did not evoke any [Ca2+]i changes. The GABA-induced increase in [Ca2+]i was observed in all retinal layers in neonatal retinal whole-mount explants. In the outer retina, the increase was seen in cone photoreceptors which were specifically labeled with peanut agglutinin (PNA). The GABA-induced increase in [Ca2+]i may provide an important mechanism for regulating cone synaptogenesis in the outer plexiform layer of the postnatal retina.