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甘氨酸能抑制灵长类动物视网膜中特定的外侧无长突细胞。

Glycinergic Inhibition Targets Specific Off Cone Bipolar Cells in Primate Retina.

机构信息

School of Optometry, University of California, Berkeley, Berkeley, CA 94720.

Helen Wills Neuroscience Institute, University of California, Berkeley, Berkeley, CA 94720.

出版信息

eNeuro. 2021 Feb 24;8(1). doi: 10.1523/ENEURO.0432-20.2020. Print 2021 Jan-Feb.

DOI:10.1523/ENEURO.0432-20.2020
PMID:33188005
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7920536/
Abstract

Adapting between scotopic and photopic illumination involves switching the routing of retinal signals between rod and cone-dominated circuits. In the daytime, cone signals pass through parallel On and Off cone bipolar cells (CBCs), that are sensitive to increments and decrements in luminance, respectively. At night, rod signals are routed into these cone-pathways via a key glycinergic interneuron, the AII amacrine cell (AII-AC). AII-ACs also provide On-pathway-driven crossover inhibition to Off-CBCs under photopic conditions. In primates, it is not known whether all Off-bipolar cell types receive functional inputs from AII-ACs. Here, we show that select Off-CBC types receive significantly higher levels of On-pathway-driven glycinergic input than others. The rise and decay kinetics of the glycinergic events are consistent with involvement of the α1 glycine receptor (GlyR) subunit, a result supported by a higher level of GLRA1 transcript in these cells. The Off-bipolar types that receive glycinergic input have sustained physiological properties and include the flat midget bipolar (FMB) cells, which provide excitatory input to the Off-midget ganglion cells (GCs; parvocellular pathway). Our results suggest that only a subset of Off-bipolar cells have the requisite receptors to respond to AII-AC input. Taken together with results in mouse retina, our findings suggest a conserved motif whereby signal output from AII-ACs is preferentially routed into sustained Off-bipolar signaling pathways.

摘要

适应暗视觉和明视觉照明涉及在杆状细胞和视锥细胞主导的回路之间切换视网膜信号的路由。在白天,视锥信号通过平行的 On 和 Off 视锥双极细胞(CBC)传递,它们分别对亮度的增加和减少敏感。在夜间,杆状细胞信号通过关键的甘氨酸能中间神经元,即 AII 无长突细胞(AII-AC),被路由到这些视锥通路中。AII-AC 还在明视觉条件下为 Off-CBC 提供 On 通路驱动的交叉抑制。在灵长类动物中,尚不清楚所有 Off 双极细胞类型是否都从 AII-AC 接收功能性输入。在这里,我们表明,某些 Off-CBC 类型接收的 On 通路驱动的甘氨酸能输入水平明显高于其他类型。甘氨酸能事件的上升和衰减动力学与α1 型甘氨酸受体(GlyR)亚基的参与一致,这一结果得到这些细胞中更高水平的 GLRA1 转录的支持。接收甘氨酸能输入的 Off-双极细胞具有持续的生理特性,包括扁平小型双极(FMB)细胞,它们为 Off-小型神经节细胞(GC;小细胞通路)提供兴奋性输入。我们的结果表明,只有一部分 Off-双极细胞具有响应 AII-AC 输入所需的受体。结合小鼠视网膜的结果,我们的发现表明存在一种保守的模式,即 AII-AC 的信号输出优先被路由到持续的 Off-双极信号通路中。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c05c/7920536/b4f07ba5fcdf/SN-ENUJ200301F008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c05c/7920536/32ec5aa8820f/SN-ENUJ200301F001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c05c/7920536/9ef0af8b3e9f/SN-ENUJ200301F005.jpg
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