The expression of GABA receptors (GABARs) was studied in frog and turtle retinae. Using immunocytochemical methods, GABA(A)Rs and GABA(C)Rs were preferentially localized to the inner plexiform layer (IPL). Label in the IPL was punctate indicating a synaptic clustering of GABARs. Distinct, but weaker label was also present in the outer plexiform layer. GABA(A)R and GABA(C)R mediated effects were studied by recording electroretinograms (ERGs) and by the application of specific antagonists. Bicuculline, the GABA(A)R antagonist, produced a significant increase of the ERG. Picrotoxin, when co-applied with saturating doses of bicuculline, caused a further increase of the ERG due to blocking of GABA(C)Rs. The putative GABA(C)R antagonist Imidazole-4-acidic acid (I4AA) failed to antagonize GABA(C)R mediated inhibition and, in contrast, appeared rather as an agonist of GABARs.

We assessed the contribution of GABAa and GABAc receptors to GABAergic effects on b- and d-wave in frog ERG in a wide range of light stimulation conditions. The amplitude of both b- and d-wave was increased during GABAa receptor blockade by bicuculline as well as during additional GABAc receptor blockade by picrotoxin. The effects of GABAa receptor blockade were more pronounced in light adaptation conditions. They strongly depended on stimulus intensity and showed considerable ON/OFF-response asymmetry. The effects of GABAc receptor blockade were more pronounced in dark adaptation conditions. They didn't vary much with stimulus intensity and showed little ON/OFF-response asymmetry.

Glycine and glycine receptors (GlyRs) were analyzed immunocytochemically in the retina of the frog Rana ridibunda. Glycine was localized to somata of glycinergic amacrine and interplexiform cells. Approximately 50% of the cells in the amacrine cell layer were found to be glycinergic. GlyRs of the inner plexiform layer (IPL) were localized to brightly fluorescent puncta, probably representing postsynaptic clusters of GlyRs. GlyR clusters were not evenly distributed across the IPL but showed patterns of stratification specific for the various GlyR subunits. Clusters containing the alpha1 subunit formed four narrow strata within the IPL. Clusters containing the alpha3 subunit were more abundant and covered the whole IPL, with a band of higher density in stratum 3. Clusters of GlyRs were also observed in the outer plexiform layer. Thus, several isoforms of synaptic GlyRs involved with different synapses and inhibitory circuits are present in the frog retina.

Perfusion of dark adapted frog eyecups with the ON pathway blocker 2-amino-4-phosphonobutyrate (APB) not only abolished the ganglion cells (GCs)' ON responses and the ERG b-wave, but it markedly potentiated the OFF responses of all ON-OFF and phasic OFF GCs and the d-wave amplitude of a simultaneously recorded ERG as well. The blockade of GABA(A) and GABA(C) receptors by picrotoxin eliminated this potentiating effect in 24 out of 41 GCs, although in the rest of the cells it did not produce any change in the APB effect. On the other hand, the d-wave potentiation was preserved during the GABAergic blockade in all experiments. Our results indicate that GABAergic transmission is involved in the inhibition exerted by the ON upon the OFF channel in part of the ON-OFF and phasic OFF GCs in the frog retina. The tonic OFF GCs probably do not receive an inhibitory input from the ON channel, because their light responses were not altered either by APB alone or by APB during blockade of GABA(A) and GABA(C) receptors.

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