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GABAergic amacrine cell feedback to bipolar cells in retina has been described, activating both GABAA and GABAC receptors. We explored whether metabotropic GABAB receptors also participate in this feedback pathway. CGP55845, a potent GABAB receptor antagonist, was employed to determine the endogenous role of these receptors. Ganglion cell EPSCs and IPSCs were monitored to measure the output of bipolar and amacrine cells. Using the tiger salamander slice preparation, we found that GABAB receptor pathways regulate bipolar cell release directly and indirectly. In the direct pathway, the GABAB receptor antagonist reduces EPSC amplitude, indicating that GABAB receptors cause enhanced glutamate release from bipolar cells to one set of ganglion cells. In the indirect pathway, the GABAB receptor antagonist reduces EPSC amplitude in another set of ganglion cells. The indirect pathway is only evident when GABAA receptors are inhibited, and is blocked by a glycine receptor antagonist. Thus, this second feedback pathway involves direct glycine feedback to the bipolar cell and this glycinergic amacrine cell is suppressed by GABAergic amacrine cells, through both GABAA and GABAB but not GABAC receptors. Overall, GABAB receptors do contribute to feedback regulation of bipolar cell transmitter release. However, unlike the ionotropic GABA receptor pathways, the metabotropic GABA receptor pathways act to enhance bipolar cell transmitter release. Furthermore, there are three discrete subsets of bipolar cell output regulated by GABAB receptor feedback (direct, indirect and null), implying three distinct, non-overlapping bipolar cell to ganglion cell circuits. |
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