Skip to main content
. 2019 Sep;60(12):4063–4073. doi: 10.1167/iovs.19-27137

Figure 4.

Figure 4

The timing of feedback inhibition from A17 amacrine cells to rod bipolar cells is shortened after 6 weeks of diabetes. (A) Representative traces of GABAergic fIPSCs averaged from two responses evoked by a 250-ms step from −60 to 0 mV recorded from rod bipolar cells are shown. The inset shows a schematic of the feedback currents, where a rod bipolar cell releases glutamate onto AMPARs (white triangle) on an A17 amacrine cell (A17) and the A17 amacrine cell releases GABA back onto GABACRs (A) and GABAARs (E). The inset in (C) shows the average GABAAR sIPSC used for deconvolution. (B) The D37 for total GABAergic fIPSCs was faster in diabetic cells (n = 13 cells from 5 mice) compared with control cells (n = 12 cells from 6 mice, P = 0.001 t-test). GABAAR (C) and GABACR-mediated (E) fIPSCs are shortened in diabetic cells (GABAAR: n = 11 cells, GABACR: n = 9 cells) compared with control cells (n = 12 cells for both receptor inputs). GABACR (D, P = 0.0001 t-test) and GABAAR-mediated (F, P = 0.005 t-test) fIPSC D37s are faster in diabetic rod bipolar cells. †P < 0.01, ‡P < 0.001.