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E.D. Eggers, P.D. Lukasiewicz; Light–evoked inhibition to bipolar cells in wild type and GABAC null mice . Invest. Ophthalmol. Vis. Sci. 2004;45(13):2193.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Visual information is divided into different signals by distinct bipolar cell classes, but it is not known how inhibition modulates these pathways. To address this we recorded GABAA, GABAC and glycine receptor–mediated light evoked IPSCs (L–IPSCs) from bipolar cells. We also examined GABAA and glycine receptor–mediated inputs in isolation using GABAC null mice. Methods: Light responses of dark–adapted bipolar cells were recorded in the whole–cell configuration from retinal slices in response to full–field illumination with a green LED. Recordings were made at the reversal potential for cation–mediated currents to isolate L–IPSCs. Receptor–specific inputs were isolated with bicuculline, TPMPA and strychnine alone and in combination. Lucifer yellow was included in the pipettes to morphologically identify bipolar cell types. Results: L–IPSCs were recorded from rod, ON cone and OFF cone bipolar cells. For each bipolar cell class from WT mice, L–IPSCs were mediated by glycine, GABAA and GABAC receptors. In null mice, only GABAA and glycine receptor–mediated L–IPSCs were present. In cells from both WT and GABAC null mice, GABAA and glycine receptor–mediated L–IPSCs were composed of bursts of small discrete IPSCs with short rise and decay times. By contrast, GABAC mediated WT responses were more prolonged and did not contain discrete events. Here we have focused on rod bipolar cells (RBCs), the most frequently encountered type. RBC L–IPSCs from the null cells were briefer than those from WT cells, suggesting that slower GABAC receptor kinetics determine the L–IPSC time course. Consistent with this notion, we found that RBC L–IPSCs were dominated by GABAC receptor–mediated inputs, with the remainder of the response composed of comparable amounts GABAA and glycine receptor–mediated input. There was no significant difference in the magnitudes of GABAA and glycine receptor–mediated currents in RBCs between WT and null mice, indicating that these receptors were not up–regulated in null mice. The intensity–response curves of RBC control L–IPSCs from WT and null mice spanned the same intensity range, but the maximum response from null cells was only 70% of WT. Conclusions: GABAA, GABAC and glycine receptors, which are present on bipolar cell axon terminals, all contribute to L–IPSCs. In WT rod bipolar cells the L–IPSCs were prolonged and dominated by GABAC receptor–mediated input. In null cells, L–IPSCs were briefer and mediated by GABAA and glycine inputs. These data indicate that postsynaptic receptor properties contribute to the L–IPSC time course, which in turn will influence the signaling from bipolar cells to ganglion cells.
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