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黑视蛋白对丘脑-皮层视觉系统辐照度编码的贡献。

Melanopsin contributions to irradiance coding in the thalamo-cortical visual system.

机构信息

Faculty of Life Sciences, University of Manchester, Manchester, United Kingdom.

出版信息

PLoS Biol. 2010 Dec 7;8(12):e1000558. doi: 10.1371/journal.pbio.1000558.

Abstract

Photoreception in the mammalian retina is not restricted to rods and cones but extends to a subset of retinal ganglion cells expressing the photopigment melanopsin (mRGCs). These mRGCs are known to drive such reflex light responses as circadian photoentrainment and pupillomotor movements. By contrast, until now there has been no direct assessment of their contribution to conventional visual pathways. Here, we address this deficit. Using new reporter lines, we show that mRGC projections are much more extensive than previously thought and extend across the dorsal lateral geniculate nucleus (dLGN), origin of thalamo-cortical projection neurons. We continue to show that this input supports extensive physiological light responses in the dLGN and visual cortex in mice lacking rods+cones (a model of advanced retinal degeneration). Moreover, using chromatic stimuli to isolate melanopsin-derived responses in mice with an intact visual system, we reveal strong melanopsin input to the ∼40% of neurons in the LGN that show sustained activation to a light step. We demonstrate that this melanopsin input supports irradiance-dependent increases in the firing rate of these neurons. The implication that melanopsin is required to accurately encode stimulus irradiance is confirmed using melanopsin knockout mice. Our data establish melanopsin-based photoreception as a significant source of sensory input to the thalamo-cortical visual system, providing unique irradiance information and allowing visual responses to be retained even in the absence of rods+cones. These findings identify mRGCs as a potential origin for aspects of visual perception and indicate that they may support vision in people suffering retinal degeneration.

摘要

哺乳动物视网膜中的光感受不仅局限于视杆细胞和视锥细胞,还扩展到表达光色素黑素视蛋白(mRGCs)的一部分视网膜神经节细胞。这些 mRGCs 已知会引起诸如昼夜节律的光顺应和瞳孔运动等反射性光反应。相比之下,直到现在,它们对传统视觉通路的贡献还没有直接评估。在这里,我们解决了这一不足。使用新的报告基因系,我们表明 mRGC 投射比以前想象的要广泛得多,并延伸到背外侧膝状体核(dLGN),即丘脑皮质投射神经元的起源。我们继续表明,这种输入支持在缺乏视杆细胞+视锥细胞的小鼠(一种视网膜退行性变的模型)的 dLGN 和视觉皮层中广泛的生理光反应。此外,使用彩色刺激物在具有完整视觉系统的小鼠中分离出黑素视蛋白衍生的反应,我们揭示了在对光阶持续激活的 LGN 中的约 40%的神经元中存在强烈的黑素视蛋白输入。我们证明这种黑素视蛋白输入支持这些神经元的放电率随辐照度增加而增加。使用黑素视蛋白敲除小鼠证实了黑素视蛋白输入是准确编码刺激辐照度所必需的。我们的数据确立了基于黑素视蛋白的光感受是丘脑皮质视觉系统的重要感觉输入源,提供独特的辐照度信息,并允许即使在缺乏视杆细胞+视锥细胞的情况下也能保留视觉反应。这些发现将 mRGCs 确定为视觉感知的潜在起源,并表明它们可能支持遭受视网膜变性的人的视力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46f4/2998442/3cd4cbf794b2/pbio.1000558.g001.jpg

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