Effect of L-glutamic acid on [14C]GABA release from isolated rat retina

Kamada, Yoshio; Mizuno, A; Matsuda, Makoto

doi:10.1016/0006-8993(81)90766-6

Cited by 10 publications

(1 citation statement)

References 16 publications

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“…We therefore conclude that, most likely there are no glutamate or aspartate receptors on the GABA accumulating neurons. Kamada et al (1981) obtained a somewhat different result in rat retina. They found a release induced by M kainic acid or 2 x M glutamic acid (but not by ~x I O -~ M aspartic acid).…”

Section: Discussionmentioning

confidence: 92%

The release of (³H)‐GABA from the rabbit retina

Agardh

Bauer

1984

Acta Physiologica Scandinavica

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The neuronal and glial release of (3H)-GABA from rabbit retina has been studied. The results indicate, that neither are there any glutamate, aspartate or glycine receptors on the GABA accumulating neurons, nor any GABA autoreceptors. (3H)-GABA was found to be released by 40 mM K+ from retinal neurons, but not from glia, and the release was not dependent on extracellular Ca++. This indicates a release from a non vesicular transmitter pool. Ouabain has been proposed as a pharmacological tool for studying the release of (3H)-GABA located in neuronal cytoplasm. However, it induced an increased release of (3H)-GABA from both neurons and glia and it is therefore unlikely that it can be used for the specific purpose of studying release from neuronal cytoplasm.

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Section: Discussionmentioning

confidence: 92%

The release of (³H)‐GABA from the rabbit retina

Agardh

Bauer

1984

Acta Physiologica Scandinavica

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Effects of excitatory amino acids, and of their agonists and antagonists on the release of neurotransmitters from the chick retina

Morán

Pasantes‐Morales

1983

J of Neuroscience Research

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Effects of glutamic, aspartic, and cysteic acid, and of kainic acid and N-methyl aspartate on the release of labeled GABA, glycine, and taurine were examined in isolated, perfused chick retina. Glutamic acid (0.5-2 mM), increased the release of 3H-GABA by more than four times and that of 14C-glycine by about two times. The release of GABA decreased 50% and that of glycine 95% in the presence of the antagonist of glutamic acid receptors, glutamate diethyl ester (300 microM). N-methyl aspartate, used as an agonist of aspartic acid receptors, preferentially increased the release of GABA (seven times) over that of glycine (three times). The stimulatory effect of N-methyl aspartate was antagonized by D-alpha-aminoadipate and by Mg. Kainic acid (10 microM) induced the release of glycine but not that of GABA. Cysteic acid failed to modify the release of any of the amino acids examined. The efflux of labeled taurine was practically unaffected by all the compounds utilized. The release of GABA by the excitatory amino acids and agonists was Ca-independent but Na-dependent, whereas the release of glycine was markedly Ca-dependent. The evidence presented here suggests that experimental conditions activating receptors of excitatory amino acids differently affect the release of inhibitory amino acids.

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GABAergic circuitry in the opossum retina: a GABA release induced by l-aspartate

2006

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Glutamate and gamma-amino butyric acid (GABA) are the major excitatory and inhibitory neurotransmitters, respectively, in the central nervous system (CNS), including the retina. Although in a number of studies the retinal source of GABA was identified, in several species, as horizontal, amacrine cells and cells in the ganglion cell layer, nothing was described for the opossum retina. Thus, the first goal of this study was to determine the pattern of GABAergic cell expression in the South America opossum retina by using an immunohistochemical approach for GABA and for its synthetic enzyme, glutamic acid decarboxylase (GAD). GABA and GAD immunoreactivity showed a similar cellular pattern by appearing in a few faint horizontal cells, topic and displaced amacrine cells. In an effort to extend the knowledge of the opossum retinal circuitry, the possible influence of glutamatergic inputs in GABAergic cells was also studied. Retinas were stimulated with different glutamatergic agonists and aspartate (Asp), and the GABA remaining in the tissue was detected by immunohistochemical procedures. The exposure of retinas to NMDA and kainate resulted the reduction of the number of GABA immunoreactive topic and displaced amacrine cells. The Asp treatment also resulted in reduction of the number of GABA immunoreactive amacrine cells but, in contrast, the displaced amacrine cells were not affected. Finally, the Asp effect was totally blocked by MK-801. This result suggests that Asp could be indeed a putative neurotransmitter in this non-placental animal by acting on an amacrine cell sub-population of GABA-positive NMDA-sensitive cells.

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Effect of L-glutamic acid on [14C]GABA release from isolated rat retina

Cited by 10 publications

References 16 publications

The release of (³H)‐GABA from the rabbit retina

The release of (³H)‐GABA from the rabbit retina

Effects of excitatory amino acids, and of their agonists and antagonists on the release of neurotransmitters from the chick retina

GABAergic circuitry in the opossum retina: a GABA release induced by l-aspartate

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Effect of L-glutamic acid on [14C]GABA release from isolated rat retina

Cited by 10 publications

References 16 publications

The release of (3H)‐GABA from the rabbit retina

The release of (3H)‐GABA from the rabbit retina

Effects of excitatory amino acids, and of their agonists and antagonists on the release of neurotransmitters from the chick retina

GABAergic circuitry in the opossum retina: a GABA release induced by l-aspartate

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Product

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The release of (³H)‐GABA from the rabbit retina

The release of (³H)‐GABA from the rabbit retina