During adaptation to an increase in environmental luminance, retinal signaling adjustments are mediated by the neuromodulator dopamine. Retinal dopamine is released with light and can affect center-surround receptive fields, the coupling state between neurons, and inhibitory pathways through inhibitory receptors and neurotransmitter release. While the inhibitory receptive field surround of bipolar cells becomes narrower and weaker during light adaptation, it is unknown how dopamine affects bipolar cell surrounds. If dopamine and light have similar effects, it would suggest that dopamine could be a mechanism for light-adapted changes. We tested the hypothesis that dopamine D1 receptor activation is sufficient to elicit the magnitude of light-adapted reductions in inhibitory bipolar cell surrounds. Surrounds were measured from OFF bipolar cells in dark-adapted mouse retinas while stimulating D1 receptors, which are located on bipolar, horizontal, and inhibitory amacrine cells. The D1 agonist SKF-38393 narrowed and weakened OFF bipolar cell inhibitory receptive fields but not to the same extent as with light adaptation. However, the receptive field surround reductions differed between the glycinergic and GABAergic components of the receptive field. GABAergic inhibitory strength was reduced only at the edges of the surround, while glycinergic inhibitory strength was reduced across the whole receptive field. These results expand the role of retinal dopamine to include modulation of bipolar cell receptive field surrounds. Additionally, our results suggest that D1 receptor pathways may be a mechanism for the light-adapted weakening of glycinergic surround inputs and the furthest wide-field GABAergic inputs to bipolar cells. However, remaining differences between light-adapted and D1 receptor–activated inhibition demonstrate that non-D1 receptor mechanisms are necessary to elicit the full effect of light adaptation on inhibitory surrounds.

中文翻译：

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多巴胺 D1 受体对视网膜双极细胞感受野的抑制成分进行差异调节

在适应环境亮度增加的过程中，视网膜信号调节是由神经调节剂多巴胺介导的。视网膜多巴胺随光释放，可影响中心周围感受野、神经元之间的耦合状态，以及通过抑制受体和神经递质释放的抑制途径。虽然在光适应期间双极细胞的抑制性感受野周围变得更窄和更弱，但尚不清楚多巴胺如何影响双极细胞周围。如果多巴胺和光具有相似的作用，则表明多巴胺可能是光适应变化的一种机制。我们检验了多巴胺 D1 受体激活足以引发抑制性双极细胞周围的光适应减少幅度的假设。从暗适应小鼠视网膜中的 OFF 双极细胞测量周围环境，同时刺激位于双极、水平和抑制性无长突细胞上的 D1 受体。D1 激动剂 SKF-38393 缩小并削弱了 OFF 双极细胞抑制性感受野，但程度与光适应不同。然而，感受野周围的减少在感受野的甘氨酸能和 GABA 能成分之间有所不同。GABA 能抑制强度仅在周围边缘降低，而甘氨酸能抑制强度在整个感受野中降低。这些结果扩大了视网膜多巴胺的作用，包括调节双极细胞感受野周围。此外，我们的研究结果表明，D1 受体途径可能是光适应减弱甘氨酸能周围输入和双极细胞最远广域 GABA 能输入的机制。然而，光适应和 D1 受体激活抑制之间的剩余差异表明，非 D1 受体机制对于引发光适应对抑制性环境的全面影响是必要的。