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本文引用的文献

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Virally delivered channelrhodopsin-2 safely and effectively restores visual function in multiple mouse models of blindness.病毒介导的通道视紫红质-2 安全有效地恢复了多种失明小鼠模型的视觉功能。
Mol Ther. 2011 Jul;19(7):1220-9. doi: 10.1038/mt.2011.69. Epub 2011 Apr 19.
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Large-scale remapping of visual cortex is absent in adult humans with macular degeneration.成年黄斑变性患者的视觉皮层不存在大规模的重新映射。
Nat Neurosci. 2011 May;14(5):649-55. doi: 10.1038/nn.2793. Epub 2011 Mar 27.
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Differential targeting of optical neuromodulators to ganglion cell soma and dendrites allows dynamic control of center-surround antagonism.光学神经调制器靶向神经节细胞体和树突的差异定位,实现了对中心-周围拮抗作用的动态控制。
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Visual function in mice with photoreceptor degeneration and transgenic expression of channelrhodopsin 2 in ganglion cells.感光细胞变性小鼠和转染表达通道视紫红质 2 的神经节细胞的视觉功能。
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Gene therapy for Leber's congenital amaurosis is safe and effective through 1.5 years after vector administration.经载体给药 1.5 年后,莱伯先天性黑蒙的基因治疗是安全有效的。
Mol Ther. 2010 Mar;18(3):643-50. doi: 10.1038/mt.2009.277. Epub 2009 Dec 1.
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Visual properties of transgenic rats harboring the channelrhodopsin-2 gene regulated by the thy-1.2 promoter.携带有 Thy-1.2 启动子调控的通道视紫红质-2 基因的转基因大鼠的视觉特性。
PLoS One. 2009 Nov 5;4(11):e7679. doi: 10.1371/journal.pone.0007679.
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Gene therapy for red-green colour blindness in adult primates.成年灵长类动物红绿色盲的基因治疗。
Nature. 2009 Oct 8;461(7265):784-7. doi: 10.1038/nature08401. Epub 2009 Sep 16.
8
Vision 1 year after gene therapy for Leber's congenital amaurosis.莱伯先天性黑矇症基因治疗1年后的视力情况。
N Engl J Med. 2009 Aug 13;361(7):725-7. doi: 10.1056/NEJMc0903652.
9
Artificial vision: needs, functioning, and testing of a retinal electronic prosthesis.人工视觉:视网膜电子假体的需求、功能及测试
Prog Brain Res. 2009;175:317-32. doi: 10.1016/S0079-6123(09)17522-2.
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Ruling out and ruling in neural codes.排除和确定神经编码。
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具有恢复正常视力能力的视网膜假体策略。

Retinal prosthetic strategy with the capacity to restore normal vision.

机构信息

Department of Physiology and Biophysics, Weill Medical College of Cornell University, New York, NY 10065, USA.

出版信息

Proc Natl Acad Sci U S A. 2012 Sep 11;109(37):15012-7. doi: 10.1073/pnas.1207035109. Epub 2012 Aug 13.

DOI:10.1073/pnas.1207035109
PMID:22891310
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3443127/
Abstract

Retinal prosthetics offer hope for patients with retinal degenerative diseases. There are 20-25 million people worldwide who are blind or facing blindness due to these diseases, and they have few treatment options. Drug therapies are able to help a small fraction of the population, but for the vast majority, their best hope is through prosthetic devices [reviewed in Chader et al. (2009) Prog Brain Res 175:317-332]. Current prosthetics, however, are still very limited in the vision that they provide: for example, they allow for perception of spots of light and high-contrast edges, but not natural images. Efforts to improve prosthetic capabilities have focused largely on increasing the resolution of the device's stimulators (either electrodes or optogenetic transducers). Here, we show that a second factor is also critical: driving the stimulators with the retina's neural code. Using the mouse as a model system, we generated a prosthetic system that incorporates the code. This dramatically increased the system's capabilities--well beyond what can be achieved just by increasing resolution. Furthermore, the results show, using 9,800 optogenetically stimulated ganglion cell responses, that the combined effect of using the code and high-resolution stimulation is able to bring prosthetic capabilities into the realm of normal image representation.

摘要

视网膜假体为视网膜退行性疾病患者带来了希望。全世界有 2000 万至 2500 万人因这些疾病而失明或面临失明,他们的治疗选择非常有限。药物疗法能够帮助一小部分人群,但对于绝大多数人来说,他们最大的希望是通过假体设备[Chader 等人综述(2009)Prog Brain Res 175:317-332]。然而,目前的假体在提供的视力方面仍然非常有限:例如,它们允许感知光点和高对比度边缘,但不能感知自然图像。为了提高假体的功能,研究人员主要集中在提高设备刺激器(电极或光遗传学换能器)的分辨率上。在这里,我们表明第二个因素也至关重要:用视网膜的神经代码驱动刺激器。我们使用小鼠作为模型系统,生成了一种包含该代码的假体系统。这极大地提高了系统的能力——远远超出了仅仅提高分辨率所能达到的水平。此外,结果表明,使用 9800 个光遗传刺激的节细胞反应,使用代码和高分辨率刺激的组合效应能够使假体功能进入正常图像表示的领域。