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T. Ichinose, P. D. Lukasiewicz; Receptor- and Glutamate Transporter-Mediated Inhibition Differently Contribute to Light-Evoked Currents in Mouse Rod Bipolar Cell Terminals. Invest. Ophthalmol. Vis. Sci. 2008;49(13):2431.
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© ARVO (1962-2015); The Authors (2016-present)
Light evokes inhibitory currents in bipolar cell (BC) terminals mediated by the activation of GABA and glycine receptors. Stimulation of glutamate transporters with glutamate also elicits an inhibitory Cl- current in rod BCs (RBCs) axon terminals, but it is unknown if this current is activated by light. Here, we investigated whether the transporter-mediated Cl- current contributed to light-evoked inhibition in bipolar cells.
Whole-cell recordings were made from BCs in dark-adapted retinal slices. BCs were voltage-clamped at 0 mV, the reversal potential for cation currents, to record Cl- mediated inhibitory currents evoked by either white full-field light or activating ON BCs directly by switching from the mGluR6 agonist AP4 to the antagonist CPPG. A cocktail of strychnine, bicuculline, and TPMPA was superfused to block glycine, GABAA and GABAC receptor (R)-mediated inhibitory currents, respectively. TBOA was used to block the glutamate transporter-associated Cl- current. Recorded bipolar cells were morphologically characterized by including sulforhodamine B in the pipette.
Dim light stimuli elicited inhibitory currents in RBCs that were eliminated by the cocktail of receptor blockers. Brighter light stimuli increased the inhibitory currents, but the larger responses were less affected by the cocktail. Inhibitory receptor antagonists reduced light sensitivity, shifting the intensity-response curve 2 log units. TBOA blocked the residual inhibitory currents, suggesting that glutamate transporter-mediated Cl- currents contributed to light-evoked inhibition in RBCs. However, in cone BCs (CBCs), the blocker cocktail abolished inhibitory currents at all light intensities. When CPPG was used to activate ON BCs and to bypass transmission in the outer plexiform layer, inhibitory currents were still observed with the blocker cocktail in RBCs, but not in CBCs. This suggested that the glutamate transporter-mediated inhibition was in the axon terminals, not in the dendrites.
We show that glutamate transporter-mediated inhibition contributed to light-evoked inhibition in RBC, but not in CBC axon terminals. This discrepancy suggests that each BC type has different complements of glutamate transporters. In RBCs, the transporter current contributes to light-evoked inhibition and is most prominent at brighter intensities.
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