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突触抑制调节视网膜中的对比度计算。

Synaptic inhibition tunes contrast computation in the retina.

作者信息

Oesch Nicholas W, Diamond Jeffrey S

机构信息

Synaptic Physiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892-3701.

出版信息

Vis Neurosci. 2019 Jan;36:E006. doi: 10.1017/S095252381900004X.

DOI:10.1017/S095252381900004X
PMID:31199207
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6578594/
Abstract

Inhibition shapes activity and signal processing in neural networks through numerous mechanisms mediated by many different cell types. Here, we examined how one type of GABAergic interneuron in the retina, the A17 amacrine cell, influences visual information processing. Our results suggest that A17s, which make reciprocal feedback inhibitory synapses onto rod bipolar cell (RBC) synaptic terminals, extend the luminance range over which RBC synapses compute temporal contrast and enhance the reliability of contrast signals over this range. Inhibition from other amacrine cells does not influence these computational features. Although A17-mediated feedback is mediated by both GABAA and GABAC receptors, the latter plays the primary role in extending the range of contrast computation. These results identify specific functions for an inhibitory interneuron subtype, as well as specific synaptic receptors, in a behaviorally relevant neural computation.

摘要

抑制作用通过多种不同细胞类型介导的众多机制塑造神经网络中的活动和信号处理。在这里,我们研究了视网膜中一种类型的γ-氨基丁酸(GABA)能中间神经元,即A17无长突细胞,如何影响视觉信息处理。我们的结果表明,A17细胞在视杆双极细胞(RBC)突触终末上形成相互反馈抑制性突触,扩展了RBC突触计算时间对比度的亮度范围,并提高了该范围内对比度信号的可靠性。来自其他无长突细胞的抑制作用不影响这些计算特征。虽然A17介导的反馈由GABAA和GABAC受体介导,但后者在扩展对比度计算范围中起主要作用。这些结果确定了抑制性中间神经元亚型以及特定突触受体在行为相关神经计算中的特定功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c69/6578594/1da6b4b36a58/nihms-1525787-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c69/6578594/f285a614a3de/nihms-1525787-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c69/6578594/318456527657/nihms-1525787-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c69/6578594/0546ba808aef/nihms-1525787-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c69/6578594/5aed0d1e15a1/nihms-1525787-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c69/6578594/1da6b4b36a58/nihms-1525787-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c69/6578594/f285a614a3de/nihms-1525787-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c69/6578594/318456527657/nihms-1525787-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c69/6578594/0546ba808aef/nihms-1525787-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c69/6578594/5aed0d1e15a1/nihms-1525787-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c69/6578594/1da6b4b36a58/nihms-1525787-f0005.jpg

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本文引用的文献

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Extrasynaptic NMDA Receptors on Rod Pathway Amacrine Cells: Molecular Composition, Activation, and Signaling.杆状通路无脊椎动物 NMDA 受体:分子组成、激活和信号转导。
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Complex inhibitory microcircuitry regulates retinal signaling near visual threshold.复杂的抑制性微电路在视觉阈值附近调节视网膜信号。
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