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首页> 外文期刊>The European Journal of Neuroscience >Dopamine modulation of rod pathway signaling by suppression of GABA(C) feedback to rod-driven depolarizing bipolar cells
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Dopamine modulation of rod pathway signaling by suppression of GABA(C) feedback to rod-driven depolarizing bipolar cells

机译：通过抑制GABA（C）反馈到杆驱动的去极化双极细胞的多巴胺调节杆途径信号

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Reducing signal gain in the highly sensitive rod pathway prevents saturation as background light levels increase, allowing the dark-adapted retina to encode stimuli over a range of background luminances. Dopamine release is increased during light adaptation and is generally accepted to suppress rod signaling in light-adapted retinas. However, recent research has suggested that dopamine, acting through D-1 receptors, could additionally produce a sensitization of the rod pathway in dim light conditions via gamma-aminobutyric acid (GABA) type C receptors. Here, we evaluated the overall activity of the depolarizing bipolar cell (DBC) population in vivo to ensure the integrity of long-distance network interactions by quantifying the b-wave of the electroretinogram in mice. We showed that dopamine, acting through D-1 receptors, reduced the amplitude and sensitivity of rod-driven DBCs during light adaptation by suppressing GABA type A receptor-mediated serial inhibition onto rod DBC GABA type C receptors. Block of D-1 receptors did not suppress rod-driven DBC sensitivity when GABA(A)-mediated serial inhibition was blocked by gabazine, suggesting that the reduction in rod-driven DBC sensitivity in the absence of D-1 receptors was due to disinhibition of serial inhibitory GABAergic circuitry rather than a direct facilitatory effect on GABA release onto rod-driven DBC GABA type C receptors. Finally, the large population of GABAergic A17 wide-field amacrine cells known to maintain reciprocal inhibition with rod DBCs could be excluded from the proposed disinhibitory circuit after treatment with 5,7-dihydroxytryptamine.
机译：降低高度敏感的杆状通路中的信号增益可防止饱和度随着背景光水平的增加而变暗，从而使适应黑暗的视网膜在一定范围的背景亮度下编码刺激。在光适应过程中，多巴胺释放增加，通常被认为可抑制光适应性视网膜中的棒信号。但是，最近的研究表明，通过D-1受体发挥作用的多巴胺还可以通过C-γ-氨基丁酸（GABA）在昏暗的光线条件下对杆状途径产生敏化作用。在这里，我们评估了体内去极化双极细胞（DBC）群体的总体活性，以通过量化小鼠视网膜电图的b波来确保长距离网络相互作用的完整性。我们表明，通过抑制GABA A型受体介导的对棒状DBC GABA C型受体的系列抑制作用，通过D-1受体起作用的多巴胺降低了杆状驱动DBC的幅度和灵敏度。当gabaazine阻断GABA（A）介导的系列抑制作用时，D-1受体的阻滞不能抑制杆驱动的DBC敏感性，这表明在缺乏D-1受体的情况下杆驱动的DBC敏感性降低了。抑制性GABA能回路的作用，而不是杆驱动DBC GABA C型受体对GABA释放的直接促进作用。最后，在用5,7-二羟基色胺治疗后，可以从拟议的去抑制回路中排除大量已知维持杆DBC相互抑制作用的GABA能A17宽视野无长突细胞。

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