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Deciphering Inhibition of Visual Plasticity by NgR1

解读 NgR1 对视觉可塑性的抑制

基本信息

批准号：
9982965
负责人：
Aaron W McGee
金额：
$ 38.5万
依托单位：
UNIVERSITY OF LOUISVILLE
依托单位国家：
美国
项目类别：
财政年份：
2012
资助国家：
美国
起止时间：
2012-05-01 至 2022-07-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/9982965
关键词：
Address Adult Alleles Amblyopia Behavioral Behavioral Assay Binocular Vision Brain Calcium Child Childhood Data Development Disease Disinhibition Electrophysiology (science)Exhibits Eye Frequencies Head Image Interneurons Knowledge Lasers Lateral Geniculate Body Lazy Eyes Location Maps Measures Mediating Mission Modeling Modification Mus Mutant Strains Mice Neurons Ocular Dominance Parvalbumins Phenotype Population Public Health Receptor Gene Recovery Research Scanning Strabismus Synapses Synaptic plasticity Testing Thalamic structure Therapeutic Therapeutic Intervention Time Vision Vision Disorders Visual Visual Acuity Visual Cortex Visual impairment Visual system structure Water brain circuitry critical period effective therapy excitatory neuron experience experimental study flexibility improved in vivo calcium imaging inhibitory neuron monocular deprivation mouse genetics mouse model neural circuit optogenetics postsynaptic programs response spatial vision targeted treatment visual deprivation visual plasticity visual processing

项目摘要

Abstract The visual system exhibits a heightened sensitivity to the quality visual experience during an interval late in development termed the `critical period'. Discordant vision during the critical period is the cause of amblyopia, a prevalent visual disorder in children. Treatment of amblyopia is most effective in children before the close of the critical period. Subsequently, the flexibility with brain circuitry diminishes in adulthood and effective therapy is more difficult. In a mouse model of amblyopia, disrupting normal vision by closing one (monocular deprivation, MD) for the duration of the critical period, but not thereafter, decreases visual acuity and perturbs the normal eye dominance of neurons in visual cortex. The nogo-66 receptor gene (ngr1) is required to close the critical period. In ngr1 mutant mice, plasticity during the critical period is normal, but it is retained in adult mice. Importantly, ngr1 mutant mice spontaneously recover visual acuity in this model of amblyopia. Our overall hypothesis is that recovery of acuity and eye dominance are independent. In the proposed research, we take advantage of this extended critical period in ngr1 mice to identify with location and mechanisms of plasticity that mediate recovery of acuity and eye dominance with a combination of conditional mouse genetics, behavioural assays, electrophysiology, sophisticated repeated in vivo calcium imaging and laser-scanning photostimulation circuit mapping. We will begin to unravel how plasticity within visual circuitry mediates recovery of visual function following early abnormal vision (MD), as well as how this plasticity is restricted to the critical period with these experiments. In addition to improving understanding of how experience-dependent plasticity changes the function of brain circuits, these studies may reveal new avenues for developing therapeutic approaches to treat amblyopia. .

摘要在后期的间隔期间，视觉系统对质量视觉体验表现出高度的敏感度发展被称为“关键时期”。关键时期视力不协调是弱视的原因，儿童普遍存在的视力障碍。弱视的治疗在儿童弱视关闭前最有效关键时期。随后，大脑回路的灵活性在成年后会减弱，并得到有效的治疗就更难了。在弱视的小鼠模型中，闭上一个(单眼)而扰乱正常视力在关键时期，但不是之后，剥夺)会降低视力和烦躁不安视皮层神经元的正常眼优势。 NOGO-66受体基因(Ngr1)是关闭关键期所必需的。在ngr1突变小鼠中，可塑性在临界期是正常的，但在成年小鼠中保留。重要的是，ngr1突变小鼠自发地在这个弱视模型中恢复视力。我们的总体假设是视力和眼睛的恢复主导权是独立的。在拟议的研究中，我们利用了这一延长的关键期 Ngr1小鼠识别调节视力和眼睛恢复的可塑性的位置和机制优势结合了条件小鼠遗传学，行为分析，电生理学，复杂的重复活体钙成像和激光扫描光刺激电路标测。我们会开始解开视觉回路内的可塑性如何调节早期视觉功能的恢复异常视觉(MD)，以及这些实验如何将这种可塑性限制在关键期。在……里面除了提高对依赖经验的可塑性如何改变大脑功能的理解之外这些研究可能会为开发治疗弱视的治疗方法提供新的途径。。

项目成果

期刊论文数量（6）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

Layer 4 Gates Plasticity in Visual Cortex Independent of a Canonical Microcircuit.

DOI：
10.1016/j.cub.2020.05.067
发表时间：
2020-08-03
期刊：
Current biology : CB
影响因子：
0
作者：
Frantz MG;Crouse EC;Sokhadze G;Ikrar T;Stephany CÉ;Nguyen C;Xu X;McGee AW
通讯作者：
McGee AW

Nogo receptor 1 is expressed by nearly all retinal ganglion cells.

DOI：
10.1371/journal.pone.0196565
发表时间：
2018
期刊：
PloS one
影响因子：
3.7
作者：
Solomon AM;Westbrook T;Field GD;McGee AW
通讯作者：
McGee AW

Nogo receptor 1 limits tactile task performance independent of basal anatomical plasticity.

DOI：
10.1371/journal.pone.0112678
发表时间：
2014
期刊：
PloS one
影响因子：
3.7
作者：
Park JI;Frantz MG;Kast RJ;Chapman KS;Dorton HM;Stephany CÉ;Arnett MT;Herman DH;McGee AW
通讯作者：
McGee AW

Multiple Roles for Nogo Receptor 1 in Visual System Plasticity.

DOI：
10.1177/1073858415614564
发表时间：
2016-12
期刊：
The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry
影响因子：
0
作者：
Stephany CÉ;Frantz MG;McGee AW
通讯作者：
McGee AW