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不同的内视网膜通路介导光反射中的杆-锥细胞输入以及小鼠行为状态的调节。

Different inner retinal pathways mediate rod-cone input in irradiance detection for the pupillary light reflex and regulation of behavioral state in mice.

机构信息

Howard Hughes Medical Institute, Universityof Iowa, Iowa City, Iowa 52242, USA.

出版信息

Invest Ophthalmol Vis Sci. 2011 Feb 1;52(1):618-23. doi: 10.1167/iovs.10-6146.

Abstract

PURPOSE

Detection of light in the eye contributes both to spatial awareness (form vision) and to responses that acclimate an animal to gross changes in light (irradiance detection). This dual role means that eye disease that disrupts form vision can also adversely affect physiology and behavioral state. The purpose of this study was to investigate how inner retinal circuitry mediating rod-cone photoreceptor input contributes to functionally distinct irradiance responses and whether that might account for phenotypic diversity in retinal disease.

METHODS

The sensitivity of the pupillary light reflex and negative masking (activity suppression by light) was measured in wild-type mice with intact inner retinal circuitry, Nob4 mice that lack ON-bipolar cell function, and rd1 mice that lack rods and cones and, therefore, have no input to ON or OFF bipolar cells.

RESULTS

An expected increase in sensitivity to negative masking with loss of photoreceptor input in rd1 was duplicated in Nob4 mice. In contrast, sensitivity of the pupillary light reflex was more severely reduced in rd1 than in Nob4 mice.

CONCLUSIONS

Absence of ON-bipolar cell-mediated rod-cone input can fully explain the phenotype of outer retina degeneration for negative masking but not for the pupillary light reflex. Therefore, inner retinal pathways mediating rod-cone input are different for negative masking and the pupillary light reflex.

摘要

目的

眼睛中的光探测不仅有助于空间感知(形态视觉),还有助于动物适应光照的大幅变化(辐照度探测)。这种双重作用意味着破坏形态视觉的眼部疾病也可能对生理和行为状态产生不利影响。本研究旨在探讨介导视杆-视锥感受器输入的内视网膜回路如何有助于功能上不同的辐照度反应,以及这是否可以解释视网膜疾病中的表型多样性。

方法

在具有完整内视网膜回路的野生型小鼠、缺乏 ON-双极细胞功能的 Nob4 小鼠和缺乏视杆和视锥且因此对 ON 或 OFF 双极细胞无输入的 rd1 小鼠中,测量瞳孔光反射和负掩蔽(光引起的活动抑制)的敏感性。

结果

rd1 中感光细胞输入缺失导致负掩蔽敏感性预期增加,这在 Nob4 小鼠中得到了复制。相比之下,rd1 小鼠的瞳孔光反射敏感性比 Nob4 小鼠降低得更严重。

结论

ON-双极细胞介导的视杆-视锥输入的缺失可以完全解释负掩蔽的外视网膜变性表型,但不能解释瞳孔光反射。因此,介导视杆-视锥输入的内视网膜通路对于负掩蔽和瞳孔光反射是不同的。

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