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E.D. Eggers, P.D. Lukasiewicz; Differential Inhibitory Signaling to Bipolar Cell Classes in Mouse Retina . Invest. Ophthalmol. Vis. Sci. 2005;46(13):1125.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Visual information is separated into parallel pathways of ON, OFF and rod signaling at the bipolar cells (BCs). It is not known if inhibitory light signaling varies among these distinct excitatory channels. To address this we recorded light–evoked inhibitory postsynaptic currents (L–IPSCs) and determined how these currents vary among rod and cone BCs. Methods: L–IPSC and spontaneous IPSC (sIPSC) recordings of BCs were made in the whole–cell configuration from dark–adapted WT and GABAC null mouse retinal slices. Light responses were stimulated by full–field illumination with a green LED. Recordings were made at the reversal potential for cation–mediated currents to isolate IPSCs. Receptor–specific inputs were isolated with GABAA, GABAC and glycine receptor antagonists alone and in combination. Lucifer yellow was included in the pipettes to morphologically identify bipolar cell types. τdecay was calculated by fitting an exponential function to the decay phase of the current. Results: To determine how inhibition varies with BC type, we recorded L–IPSCs from rod, ON and OFF cone BCs. We found that rod BC L–IPSCs had a significantly longer τdecay than L–IPSCs from ON and OFF cone BCs. To determine if this could be explained by differences in receptor inputs, we recorded L–IPSCs mediated by isolated GABAC, GABAA and glycine receptors. GABAC receptor–mediated L–IPSCs had the longest τdecay, followed by glycine receptor–mediated L–IPSCs and then GABAA receptor–mediated L–IPSCs. We also found that glycine receptor–mediated sIPSCs had a significantly slower τdecay than GABAA receptor–mediated sIPSCs, suggesting that the time–course differences of L–IPSCs are due to receptor properties. Thus, these three inhibitory receptor types potentially mediate distinct temporal channels. As GABAC receptors have the slowest timecourse, prolonged L–IPSCs observed in rod BCs could be caused by GABAC receptor inputs. We found that rod BC L–IPSCs have a significantly longer τdecay in WT than in GABAC null mice. In addition, in GABAC null mice we saw no significant difference between the τdecay of L–IPSCs from rod and ON cone BCs, suggesting that the difference in their τdecay is mediated by GABAC receptors. Conclusions: We found that different temporal inhibitory pathways could be mediated by GABAC, GABAA and glycine receptors in mouse BCs. GABAC receptors prolong L–IPSCs in BCs, and rod BCs receive more GABAC mediated input, causing their decay times to be longer. It is possible that the prolonged inhibition in rod BCs matches these currents to the relatively slow rod–mediated inputs they receive.
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