Gaba Release Mechanism in the Golden Hamster Retina

Abstract

High K+ medium and glutamate elicited a significant [3H]-GABA release in the golden hamster retina. High K+ -induced GABA release was largely calcium-dependent, while the effect of glutamate was Ca2+ -independent. After replacing Na+ by Li+, glutamate-evoked [3H]-GABA release was abolished, while high K+ -evoked release remained unchanged. The effect of glutamate was completely blocked by DNQX but not by APV. Furthermore, kainate induced [3H]-GABA release, whereas NMDA was ineffective. Assessment of endogenous GABA efflux further confirmed results obtained for [3H]-GABA. GABA-like immunoreactivity was observed in amacrine cells, in neurons localized in ganglion cell layer, as well as in fibers and terminals at the inner plexiform layer. In addition a few horizontal cells showed GABA-like immunolabeling. The present results suggest the existence of at least two pools of GABA in the hamster retina, compatible with both vesicular and carrier-mediated mechanisms of transmitter release, being the amacrine cells the main gabaergic source in this tissue.

Effect of neurosteroids on the retinal gabaergic system and electroretinographic activity in the golden hamster

“…1994), in the hamster retina P450scc‐like immunolabelling was strong in this layer. Remarkably, the localization of this key steroidogenic enzyme in the hamster closely coincides with the retinal region in which GABA is found in greatest abundance (López‐Costa et al . 1999).…”

“…1994; Shibuya et al . 2003), it is improbable that this effect could account for the increase in GABA release, as in the hamster retina this parameter is not affected by NMDA (López‐Costa et al . 1999).…”

“…1986; Yazulla 1986; Chun and Wassle 1989; Johnson and Vardi 1998). In the golden hamster retina, we have demonstrated GABA‐like immunoreactivity in amacrine cells, in neurons localized to the ganglion cell layer, in fibres and terminals within the inner plexiform layer, as well as in a few horizontal cells (López‐Costa et al . 1999).…”

Vesicular γ‐aminobutyric acid transporter expression in amacrine and horizontal cells

“…Numerous amacrine and displaced amacrine cells contain GABA or glycine and express the GABA synthetic enzymes glutamic acid decarboxylase 65 and 67 (GAD 65 and GAD 67 ) and the GABA plasma membrane transporters-1 and -3 (GAT-1 and GAT-3) or the glycine plasma membrane transporter-1 (GlyT-1) (Hendrickson et al, 1988;Pourcho and Owczarzak, 1991;Johnson et al, 1996;Crook and Pow, 1997;Menger et al, 1998;Vardi et al, 1998;. Furthermore, GABA-and glycineimmunoreactive amacrine cell terminals have synaptic contacts with accumulations of synaptic vesicles, suggesting that these cells release GABA or glycine by conventional vesicular mechanisms (Hendrickson et al, 1988;Chun and Wä ssle, 1989;Grü nert and Wä ssle, 1990;Lopez-Costa et al, 1999).…”

Effect of GABA on Melatonin Content in Golden Hamster Retina

“…In the golden hamster retina, GABA-like immunoreactivity is located in amacrine cells, displaced amacrine cells, and a few horizontal cells as well as in fibers and terminals at the inner plexiform layer (Lbpez-Costa et al, 1998). The distribution of GABA, receptors among the different cell types of the retina is not yet known in detail, but the available results indicate that those GABAergic receptors exist in at least some members of each basic type of retinal cells (for review, see Ishida, 1992).…”