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- W1488795370 abstract "Glycine receptors (GlyRs) of displaced amacrine cells of the mouse retina were analysed using whole cell recordings and immunocytochemical staining with subunit‐specific antibodies. During the recordings the cells were filled with a fluorescent tracer and 11 different morphological types could be identified. The studies were performed in wild‐type mice and in mutant mice deficient in the GlyRα1 ( Glra1 spd‐ot , ‘oscillator’ mouse), the GlyRα2 ( Glra2 −/− ) and the GlyRα3 subunit ( Glra3 −/− ). Based on their responses to the application of exogenous glycine in the retinas of wild‐type and mutant mice, the cells were grouped into three major classes: group I cells (comprising the morphological types MA‐S5, MA‐S1, MA‐S1/S5, A17, PA‐S1, PA‐S5 and WA‐S1), group II cells (comprising the morphological types PA‐S4, WA‐S3 and WA‐multi) and ON‐starburst cells. For further analysis, spontaneous inhibitory postsynaptic currents (sIPSCs) were measured both in wild‐type and mutant mouse retinas. Glycinergic sIPSCs and glycine induced currents of group I cells remained unaltered across wild‐type and the three mutant mice (mean decay time constant of sIPSCs, τ∼25 ms). Group II cells showed glycinergic sIPSCs and glycine induced currents in wild‐type, Glra1 spd‐ot and Glra3 −/− mice (τ∼25 ms); however, glycinergic currents were absent in group II cells of Glra2 −/− mice. Glycine induced currents and sIPSCs recorded from ON‐starburst amacrine cells did not differ significantly between wild‐type and the mutant mouse retinas (τ∼50–70 ms). We propose that GlyRs of group II cells are dominated by the α2 subunit; GlyRs of ON‐starburst amacrine cells appear to be dominated by the α4 subunit." @default.
- W1488795370 created "2016-06-24" @default.
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- W1488795370 creator A5030830335 @default.
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- W1488795370 date "2009-07-30" @default.
- W1488795370 modified "2023-10-17" @default.
- W1488795370 title "Glycinergic input of widefield, displaced amacrine cells of the mouse retina" @default.
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- W1488795370 doi "https://doi.org/10.1113/jphysiol.2009.171207" @default.
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