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本文引用的文献

1
An integrated approach to diabetic retinopathy research.糖尿病视网膜病变研究的综合方法。
Arch Ophthalmol. 2011 Feb;129(2):230-5. doi: 10.1001/archophthalmol.2010.362.
2
Validation of structural and functional lesions of diabetic retinopathy in mice.小鼠糖尿病视网膜病变结构和功能损伤的验证
Mol Vis. 2010 Oct 19;16:2121-31.
3
Age-related deterioration of rod vision in mice.小鼠的杆状视觉与年龄相关的退化。
J Neurosci. 2010 Aug 18;30(33):11222-31. doi: 10.1523/JNEUROSCI.4239-09.2010.
4
Visual dysfunction associated with diabetic retinopathy.与糖尿病视网膜病变相关的视觉功能障碍。
Curr Diab Rep. 2010 Oct;10(5):380-4. doi: 10.1007/s11892-010-0132-4.
5
Global transcriptional programs in peripheral nerve endoneurium and DRG are resistant to the onset of type 1 diabetic neuropathy in Ins2 mice.周围神经内膜和背根神经节中的全球转录程序对 1 型糖尿病神经病变在 Ins2 小鼠中的发生具有抗性。
PLoS One. 2010 May 26;5(5):e10832. doi: 10.1371/journal.pone.0010832.
6
Lack of both bradykinin B1 and B2 receptors enhances nephropathy, neuropathy, and bone mineral loss in Akita diabetic mice.缓激肽B1和B2受体均缺失会加重秋田糖尿病小鼠的肾病、神经病变和骨矿物质流失。
Proc Natl Acad Sci U S A. 2010 Jun 1;107(22):10190-5. doi: 10.1073/pnas.1005144107. Epub 2010 May 17.
7
Initiation of the optokinetic response (OKR) in mice.小鼠视动反应(OKR)的启动。
J Vis. 2010 Jan 29;10(1):13.1-17. doi: 10.1167/10.1.13.
8
Neuritic dystrophy and neuronopathy in Akita (Ins2(Akita)) diabetic mouse sympathetic ganglia.阿基塔(Ins2(Akita))糖尿病小鼠交感神经节中的神经炎性营养不良和神经元病。
Exp Neurol. 2009 Mar;216(1):207-18. doi: 10.1016/j.expneurol.2008.11.019. Epub 2008 Dec 10.
9
Regulation of pancreatic beta cell mass by neuronal signals from the liver.肝脏神经元信号对胰腺β细胞质量的调节。
Science. 2008 Nov 21;322(5905):1250-4. doi: 10.1126/science.1163971.
10
The role of Humphrey Matrix testing in the early diagnosis of retinopathy in type 1 diabetes.汉弗莱矩阵测试在1型糖尿病视网膜病变早期诊断中的作用。
Br J Ophthalmol. 2008 Dec;92(12):1656-60. doi: 10.1136/bjo.2008.143057. Epub 2008 Oct 1.

糖尿病 Ins2Akita 小鼠模型的光感受器运动行为的空间频率阈值和对比敏感度受损。

Spatial frequency threshold and contrast sensitivity of an optomotor behavior are impaired in the Ins2Akita mouse model of diabetes.

机构信息

Department of Physiology and Center for Biomedical Neuroscience, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, United States.

出版信息

Behav Brain Res. 2012 Jan 15;226(2):601-5. doi: 10.1016/j.bbr.2011.09.030. Epub 2011 Sep 28.

DOI:10.1016/j.bbr.2011.09.030
PMID:21963766
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3298119/
Abstract

Diabetic retinopathy can lead to progressive loss of vision and is a leading cause of blindness. The Ins2(Akita) mouse model of diabetes develops significant retinal and systemic pathology, but how these affect visual behavior is unknown. Here, we show that Ins2(Akita) mice have progressive, quantifiable vision deficits in an optomotor behavior. This mouse line is a promising model in which to understand the contribution of retinal neuronal injury during the chronic hyperglycemia and hypoinsulinemia of diabetes to deficits in vision.

摘要

糖尿病视网膜病变可导致视力逐渐丧失,是失明的主要原因。Ins2(Akita) 糖尿病小鼠模型会出现显著的视网膜和全身病理变化,但这些变化如何影响视觉行为尚不清楚。在这里,我们展示了 Ins2(Akita) 小鼠在光感受器行为中存在进行性、可量化的视觉缺陷。该小鼠品系是一个很有前途的模型,可以了解在糖尿病的慢性高血糖和胰岛素缺乏期间视网膜神经元损伤对视功能缺陷的贡献。