Name: the rodent model of nonarteritic anterior ischemic optic neuropathy (rnaion)
Uploaded: 2016-11-20T13:00:00.000+00:00
Duration: 6 min 49 s
Description: Watch this Scientific Journal Video about The Rodent Model of Nonarteritic Anterior Ischemic Optic Neuropathy rNAION at JoVE.com

我们感谢谁对这个模型工作的许多学生和研究人员，以提高其有效性，并了解其作用机制。特别感谢博士的。玛丽·约翰逊（马里兰大学巴尔的摩分校），Nitza登堡 - 科恩（施奈德曼儿童医院，佩塔提克瓦-Tikva的，以色列），张朝阳（爱因斯坦医学院，布朗克斯，NY），和Valerie Touitou（总医院Salpetrie，法国巴黎）。这项研究是由RO1 EY015304为SLB部分资助。

该协议被批准马里兰机构动物护理和利用委员会的大学（IACUC，巴尔的摩，MD，USA） 1.实验装置<ol><li>使由透明光学级圆形直径7毫米的有机玻璃，厚3mm的定制设计的隐形眼镜。切用钻床的圆形透镜。使用标准钻头以使内曲面，最后抛光使用超微粒度（3000分之1000）的接触透镜抛光外侧和内侧曲线。 </li><li>预先在pH 7.4的磷酸盐缓冲盐水（PBS）制备的2.5mM玫瑰红（RB），过滤消毒用0.45微米注射器式滤器并储存在-20℃1ml等份在一个不透光的容器中长达6个月。 注意:使用白化远系繁殖的雄性动物，如只SD的最小的应变依赖性反应的差异，使增加的易于诱导，并减少可与发情个循环发生的变异NG女性。 </li><li>设置了倍频钕钇铝石榴石（FD-YAG）眼科医疗激光，其产生532nm的激光。安装使用标准的眼科激光适配器上海牙，斯特赖特眼科裂隙灯激光。这市售设备时使动物的眼睛和激光光斑应用程序同时可视化。激光医疗也有适当的对焦和中心定位使用相同的光斑尺寸激光感应瞄准光束。激光功率参数如下: <ol><li>对于大鼠rNAION感应:使用500微米的光斑尺寸/ 50毫瓦的激光功率/ 1000毫秒时间/ 1000毫秒间隔。 </li><li>对于鼠标rNAION感应:改变光斑大小为300微米的较小的视盘和离开其他参数相同的鼠设置。 </li><li>经常使用的激光功率计，以保证激光功率输出。 </li></ol></li></ol> 2.实验步骤<ol><li>打开激光功率并设置适当的激光参数。暖激光使用前至少五分钟。 </li><li>称重动物，以确定氯胺酮/赛拉嗪和RB染料的适当剂量。由80毫克/毫升氯胺酮和4mg / ml的甲苯噻嗪1毫升/千克混合物的腹膜内注射麻醉动物。 </li><li>离开动物在笼子里加热，直至完全麻醉。检查到厌恶刺激（尾或脚趾捏）没有反应。检查动物麻醉深度每10分钟。 </li><li>扩张动物的瞳孔以1％托并用0.5％丙对卡因麻醉眼的表面上。如果使用着色的动物，如龙埃文斯，2.5％neosynephrine滴眼液将增加瞳孔扩大。 </li><li>用剪刀剪下靠近枪口上侧面的胡须被诱导，以避免遮挡住了。 </li><li>把1％甲基纤维素或其他眼科耦合下降到定制的隐形眼镜内的一滴，然后应用到镜头Ť他眼睛鼠。 </li><li>放置动物调至裂隙灯的高度的平台上。使眼球垂直于裂隙灯和激光束以45°角设置动物的头。 </li><li>通过眼科裂隙灯形象化的眼球。确保瞄准光束的大小是否合适，以及重点突出，直接集中在可视化视神经。速度方面地安装在裂隙灯眼睛件与定制适配器之一 - 使用数字照相机具有高的ASA（2,000 1,200）拍摄视网膜眼底。 注意:要看到脉络膜血管的能力，揭示了视网膜的透明度。这是为了能够检测后视网膜缺血，如果它发生可混淆的解释的重要标志。 rNAION是视神经缺血，这导致分离的RGC损失，而在视网膜损伤视网膜缺血的结果影响到所有视网膜内层的细胞。 </li><li>任选地，进一步的图像在视网膜和视神经使用谱域光学相干断层扫描（SD-10月8日），以评估未引起注意。扫描连接面 （ 图3B），以及通过在视网膜（ 图3C）7剖扫描。对SD-OCT成像使用用于激光感应同一隐形眼镜。 </li><li>注射1毫升/公斤静脉注射RB尾静脉，并等待30秒，然后激活激光功率。这次延迟使得RB在整个循环均匀分布。我们用一个50毫瓦的激光脉冲在同一秒/脉冲。更大的能量（≥60 MW）会损害视网膜或引起视网膜血管缺血。 注意:确保每个人都有一双合适的阻塞波长的激光安全过滤眼镜，以防止杂散激光进入研究者的眼球。 注意:激光给药必须迅速静脉注射RB注射后给予因为染料被从循环迅速消灭。较长的激光诱导，在更严重的视神经缺血。一般情况下，动物被赋予7 - 12秒脉冲在快速连续。激光的与循环染料的接触使视神经血管美丽的金色的光晕，可以通过裂隙灯（ 图4B）可见。这证明了染料全身注射和分布到血流中。如果发光微弱，或根本（ 图4A）无，染料不静脉注射。在这种情况下，不立即给予第二次注射，因为动物将需要用于再注入之前至少两天恢复。 </li><li>感应后立即移除隐形眼镜。覆盖眼科三联抗生素（抗生素软膏/多粘菌素/杆菌肽）软膏地塞米松双眼，然后将动物在严密观察下一个安置笼37℃加热垫，直到完全康复。 <ol><li>清洁隐形眼镜用蒸馏水W¯¯亚特并擦干用非研磨性清洁布以备将来使用。 </li><li>诱导两天后评估由双方眼底彩色照相和SD-OCT分析8视神经水肿。 注:视神经水肿程度的比较给出了视神经缺血的严重程度的估计。在两天内，视神经盘缘模糊，以及视网膜静脉稍微扩张，与对侧（未诱导）眼相比较。两个，其余四周进行电图（ERG）和闪光视觉诱发电位（VEP 11）发布诱导电分析。 </li></ol></li></ol>

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作者什么都没有透露。

虽然有若干的视神经损伤（视神经损伤12，视神经横断13和PION 14）的机型，rNAION模型是人性化，适应大鼠和小鼠。它更类似于NAION的人体临床状况。这种情况包括渐进式前视神经水肿，前路视神经骨筋膜室综合征，局灶性脑缺血轴突的，孤立的视网膜神经节细胞轴突的破坏和损失在延长的时间过程。目前报告给出了rNAION感应适当的步骤，诱导期间讨论的潜在问题，并且描述...

非动脉炎性前部缺血性视神经病（NAION）是视神经（ON）1的前部的局灶性缺血病变。 NAION是在50 2岁以上的个体突然视神经相关的视力丧失的最常见的原因。机理被认为是，其导致神经内水肿一个室综合征，并且使得毛细管视神经内供给轴突压缩3。 因为在ON实际上是一种中枢神经系统（CNS）道，啮齿动物NAION（rNAION）模型可以用于机制和响应研究分离的CNS白质笔。因此，rNAION模型可能在解剖与白质中风相关的损害相关的许多问题非常有用。它可以用来评估在白质行程不同神经保护策略和代理。 之一的模型的最吸引人的特点是，它是无痛，无创的过程。激光功率可被调节，以产生不同程度的局部缺血损伤的。另一个特点是，它依赖于激光诱导超氧自由基损伤毛细血管内皮，产生累进毛细管功能障碍。它是被认为是非常相似的，导致NAION机制此功能障碍和渐进水肿。研究已经表明，它不会导致直接毛细管凝结，但通过至少两种机制工作的:过氧化物诱导的死亡和一些毛细管的剥离内皮细胞4，和激活的B细胞的的NFkB（核因子kappa轻链增强剂）相关的炎症性上调在剩余的内皮，具有增加的跨细胞膜流体输送入间质5。视神经毛细血管受压所致间液积聚导致视神经缺血头的关闭。示意图图片所示图2，rNAION模型可在大鼠和小鼠物种6,7-都可以使用，并可以在其严重性的程度而改变，从轻微损伤视神经的完整，但无痛破坏和视网膜等视网膜中央动脉阻塞（CRAO）。

<table><tbody><tr><td>50 mW 532 nm laser</td><td>Iridex</td><td></td><td>Standard Ophthalmic Laser</td></tr><tr><td>0 - 100 mW 532 nm laser</td><td>Laserglow technologies</td><td></td><td>Substitute for iridex</td></tr><tr><td>Laser slit lamp adapter</td><td>Iridex</td><td></td><td>SMA coupled adapter for laser output</td></tr><tr><td>Coherent Fieldmate laser meter with thermopile sensor</td><td>Coherent</td><td></td><td>others also appropriate</td></tr><tr><td>Ophthalmic Examing Slit lamp biomicroscope</td><td>Various</td><td></td><td>Haag-Streit is the best; cheaper versions available on ebay</td></tr><tr><td>Rose Bengal</td><td>Sigma</td><td>330000-1G</td><td>Photoinducing agent</td></tr><tr><td>Fundus Contact lens or glass cover slip</td><td>custom/Cantor and Nissel (UK)</td><td></td><td>Custom designed planoconvex plastic lens for eye exam and induction</td></tr><tr><td>Tropicamide 1%</td><td></td><td></td><td></td></tr><tr><td>Tamiya polishing compound</td><td>Tamiya, INC</td><td>87068</td><td>polishing contact lens</td></tr><tr><td>2.5% Hypromellose (Goniovisc)/1% Methycellulose</td><td>HUB Pharmaceuticals</td><td></td><td>contact lens coupling agent</td></tr><tr><td>2.5% Neosynephrine Ophthalmic drops</td><td>Alcon labs</td><td></td><td>pupil dilating agent</td></tr><tr><td>Tropicamide 1%</td><td>Alcon labs</td><td></td><td>pupil dilating agent</td></tr><tr><td>0.5% Proparacaine</td><td>Alcon labs</td><td></td><td>topical Anesthetic</td></tr><tr><td>30 G fused needle insulin syringe</td><td>Various</td><td>Various</td><td>for intravenous injection of rose bengal</td></tr><tr><td>Ophthamic Antibiotic ointment with dexamethasone added (Triple antibiotic ointment)</td><td>Various</td><td>Various</td><td>Apply after induciton to minimize corneal scarring</td></tr><tr><td>Heidelberg Corporation Spectral domain-Optical Coherence Tomograph</td><td>Heidelberg Corporation</td><td></td><td>For Optical coherence measurements baseline and post-induction; not essential for induction</td></tr></tbody></table>

the rodent model of nonarteritic anterior ischemic optic neuropathy (rnaion)

Nonarteritic anterior ischemic optic neuropathy (NAION) is a focal ischemic lesion of the optic nerve that affects 1/700 individuals throughout their lifetime. NAION results in optic nerve edema, selective loss of the retinal ganglion cell neurons (RGCs) and atrophy of the optic nerve. A rodent model of NAION that expresses most NAION features and sequelae has been developed, which is applicable to both rats and mice. This model utilizes a focal laser application of 532 nm wavelength to illuminate a photoactive dye, Rose Bengal (RB), to cause capillary damage and leakage at the targeted anterior optic nerve (the laminar region). After rNAION induction, there is an early optic nerve ischemia, optic nerve edema, and intraneural inflammation, followed by selective RGC and axonal loss. Since the optic nerve is a CNS white matter tract, the rNAION model is applicable to mechanistic studies of selective white matter ischemia, as well as neuroprotective analyses and short and long-term mechanisms of glial and neuronal response to ischemia.

<html>接触透镜使中心视网膜可视（ 图1）。的焦点激光光斑照射在视网膜的后面视盘（ 图2）。正常未诱导视网膜示出由裂隙灯生物显微镜（ 图3A）和在SD-OCT（ 图3B和3C）成像。期间激光感应，当没有染料存在于循环，激光不会导致容器和磁盘荧光（ 图4A）。静脉RB和在一个金黄色荧光视盘结果对视神经（ <stron...

Watch this Scientific Journal Video about The Rodent Model of Nonarteritic Anterior Ischemic Optic Neuropathy rNAION at JoVE.com

The Rodent Model of Nonarteritic Anterior Ischemic Optic Neuropathy rNAION

The following report describes how to replicate the rodent model of nonarteritic anterior ischemic optic neuropathy (rNAION), using the appropriate dye, contact lens and laser parameters. We also reveal the appropriate steps for evaluating the rNAION lesion in vivo.

非动脉炎性前部缺血性视神经病变的啮齿动物模型（rNAION）

Nonarteritic anterior ischemic optic neuropathy (NAION) is a focal ischemic lesion of the optic nerve that affects 1/700 individuals throughout their ...

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The Rodent Model of Nonarteritic Anterior Ischemic Optic Neuropathy (rNAION)

8.9K 次观看.  University of Maryland-Baltimore School of Medicine. The following report describes how to replicate the rodent model of nonarteritic anterior ischemic optic neuropathy (rNAION), using the appropriate dye, contact lens and laser parameters. We also reveal the appropriate steps for evaluating the rNAION lesion in vivo.

视频: The Rodent Model of Nonarteritic Anterior Ischemic Optic Neuropathy rNAION

An Optic Nerve Crush Injury Murine Model to Study Retinal Ganglion Cell Survival

Injury to the optic nerve can lead to axonal degeneration, followed by a gradual death of retinal ganglion cells (RGCs), which results in irreversible vision loss. Examples of such diseases in human include traumatic optic neuropathy and optic nerve degeneration in glaucoma. It is characterized by typical changes in the optic nerve head, progressive optic nerve degeneration, and loss of retinal ganglion cells, if uncontrolled, leading to vision loss and blindness.
The optic nerve crush (ONC) injury mouse model is an important experimental disease model for traumatic optic neuropathy, glaucoma, etc. In this model, the crush injury to the optic nerve leads to gradual retinal ganglion cells apoptosis. This disease model can be used to study the general processes and mechanisms of neuronal death and survival, which is essential for the development of therapeutic measures. In addition, pharmacological and molecular approaches can be used in this model to identify and test potential therapeutic reagents to treat different types of optic neuropathy.
Here, we provide a step by step demonstration of (I) Baseline retrograde labeling of retinal ganglion cells (RGCs) at day 1, (II) Optic nerve crush injury at day 4, (III) Harvest the retinae and analyze RGC survival at day 11, and (IV) Representative result.

This protocol shows how to retrogradely label retinal ganglion cells, and how to subsequently make an optic nerve crush injury in order to analyze retinal ganglion cell survival and apoptosis. It is an experimental disease model for different types of optic neuropathy, including glaucoma.

一个视神经挤压伤的小鼠模型，研究视网膜神经节细胞生存

Injury to the optic nerve can lead to axonal degeneration, followed by a gradual death of retinal ganglion cells (RGCs), which results in irreversible ...

科研

神经科学

A Laser-induced Mouse Model of Chronic Ocular Hypertension to Characterize Visual Defects

Glaucoma, frequently associated with elevated intraocular pressure (IOP), is one of the leading causes of blindness. We sought to establish a mouse model of ocular hypertension to mimic human high-tension glaucoma. Here laser illumination is applied to the corneal limbus to photocoagulate the aqueous outflow, inducing angle closure. The changes of IOP are monitored using a rebound tonometer before and after the laser treatment. An optomotor behavioral test is used to measure corresponding changes in visual capacity. The representative result from one mouse which developed sustained IOP elevation after laser illumination is shown. A decreased visual acuity and contrast sensitivity is observed in this ocular hypertensive mouse. Together, our study introduces a valuable model system to investigate neuronal degeneration and the underlying molecular mechanisms in glaucomatous mice.

Chronic ocular hypertension is induced using laser photocoagulation of the trabecular meshwork in mouse eyes. The intraocular pressure (IOP) is elevated for several months after laser treatment. The decrease of visual acuity and contrast sensitivity of experimental animals are monitored using the optomotor test.

激光诱导的慢性高眼压表征视觉缺陷的小鼠模型

Glaucoma, frequently associated with elevated intraocular pressure (IOP), is one of the leading causes of blindness. We sought to establish a mouse model ...

医学

Rat Model of Photochemically-Induced Posterior Ischemic Optic Neuropathy

Posterior Ischemic optic neuropathy (PION) is a sight-devastating disease in clinical practice. However, its pathogenesis and natural history have&#160;remained poorly understood. Recently, we developed a reliable, reproducible animal model of PION and tested the treatment effect of some neurotrophic factors in this model1. The purpose of this video is to demonstrate our photochemically induced model of posterior ischemic optic neuropathy, and to evaluate its effects with retrograde labeling of retinal ganglion cells. Following surgical exposure of the posterior optic nerve, a photosensitizing dye, erythrosin B, is intravenously injected and a laser beam is focused onto the optic nerve surface. Photochemical interaction of erythrosin B and the laser during irradiation damages the vascular endothelium, prompting microvascular occlusion mediated by platelet thrombosis and edematous compression. The resulting ischemic injury yields a gradual but pronounced retinal ganglion cell dieback, owing to a loss of axonal input - a remote, injury-induced and clinically relevant outcome. Thus, this model provides a novel platform to study the pathophysiologic course of PION,&#160;and can be further optimized for testing therapeutic approaches for optic neuropathies as well as other CNS ischemic diseases.

The goal of this protocol is to photochemically induce ischemic injury to the posterior optic nerve in rat. This model is critical to studies of the pathophysiology of posterior ischemic optic neuropathy, and therapeutic approaches for this and other optic neuropathies, as well as of other CNS ischemic diseases.

光化学诱导后部缺血性视神经病变的大鼠模型

Posterior Ischemic optic neuropathy (PION) is a sight-devastating disease in clinical practice. However, its pathogenesis and natural history ...

A Mouse Model for Laser-induced Choroidal Neovascularization

The mouse laser-induced choroidal neovascularization (CNV) model has been a crucial mainstay model for neovascular age-related macular degeneration (AMD) research. By administering targeted laser injury to the RPE and Bruch&#8217;s membrane, the procedure induces angiogenesis, modeling the hallmark pathology observed in neovascular AMD. 
First developed in non-human primates, the laser-induced CNV model has come to be implemented into many other species, the most recent of which being the mouse. Mouse experiments are advantageously more cost-effective, experiments can be executed on a much faster timeline, and they allow the use of various transgenic models. The miniature size of the mouse eye, however, poses a particular challenge when performing the procedure. Manipulation of the eye to visualize the retina requires practice of fine dexterity skills as well as simultaneous hand-eye-foot coordination to operate the laser. However, once mastered, the model can be applied to study many aspects of neovascular AMD such as molecular mechanisms, the effect of genetic manipulations, and drug treatment effects. 
The laser-induced CNV model, though useful, is not a perfect model of the disease. The wild-type mouse eye is otherwise healthy, and the chorio-retinal environment does not mimic the pathologic changes in human AMD. Furthermore, injury-induced angiogenesis does not reflect the same pathways as angiogenesis occurring in an age-related and chronic disease state as in AMD.
Despite its shortcomings, the laser-induced CNV model is one of the best methods currently available to study the debilitating pathology of neovascular AMD. Its implementation has led to a deeper understanding of the pathogenesis of AMD, as well as contributing to the development of many of the AMD therapies currently available.

Here, we present the mouse laser-induced choroidal neovascularization (CNV) protocol, an experimental model that re-creates the vascular hallmarks of neovascular age-related macular degeneration (AMD). Once mastered, it can reliably and effectively induce CNV as a model system to test various experimental measures.

小鼠模型的激光诱导脉络膜新生血管

The mouse laser-induced choroidal neovascularization (CNV) model has been a crucial mainstay model for neovascular age-related macular degeneration (AMD) ...

Glaucoma-inducing Procedure in an In Vivo Rat Model and Whole-mount Retina Preparation

Glaucoma is a disease of the central nervous system affecting retinal ganglion cells (RGCs). RGC axons making up the optic nerve carry visual input to the brain for visual perception. Damage to RGCs and their axons leads to vision loss and/or blindness. Although the specific cause of glaucoma is unknown, the primary risk factor for the disease is an elevated intraocular pressure. Glaucoma-inducing procedures in animal models are a valuable tool to researchers studying the mechanism of RGC death. Such information can lead to the development of effective neuroprotective treatments that could aid in the prevention of vision loss. The protocol in this paper describes a method of inducing glaucoma - like conditions in an in vivo rat model where 50 &#181;l of 2 M hypertonic saline is injected into the episcleral venous plexus. Blanching of the vessels indicates successful injection. This procedure causes loss of RGCs to simulate glaucoma. One month following injection, animals are sacrificed and eyes are removed. Next, the cornea, lens, and vitreous are removed to make an eyecup. The retina is then peeled from the back of the eye and pinned onto sylgard dishes using cactus needles. At this point, neurons in the retina can be stained for analysis. Results from this lab show that approximately 25% of RGCs are lost within one month of the procedure when compared to internal controls. This procedure allows for quantitative analysis of retinal ganglion cell death in an in vivo rat glaucoma model.

Glaucoma-inducing Procedure in an In Vivo Rat Model and Whole-mount Retina Preparation

Glaucoma is characterized by damage to retinal ganglion cells. Inducing glaucoma in animal models can provide insight into the study of this disease. Here, we outline a procedure that induces loss of RGCs in an in vivo rat model and demonstrates the preparation of whole-mount retinas for analysis.

青光眼诱导在程序<em&gt;在体内</em&gt;大鼠模型和全安装视网膜准备

Glaucoma is a disease of the central nervous system affecting retinal ganglion cells (RGCs). RGC axons making up the optic nerve carry visual input to the ...

A Mouse Model of Retinal Ischemia-Reperfusion Injury Through Elevation of Intraocular Pressure

Retinal ischemia-reperfusion (I/R) is a pathophysiological process contributing to cellular damage in multiple ocular conditions, including glaucoma, diabetic retinopathy, and retinal vascular occlusions. Rodent models of I/R injury are providing significant insights into mechanisms and treatment strategies for human I/R injury, especially with regard to neurodegenerative damage in the retinal neurovascular unit. Presented here is a protocol for inducing retinal I/R injury in mice through elevation of intraocular pressure (IOP). In this protocol, the ocular anterior chamber is cannulated with a needle, through which flows the drip of an elevated saline reservoir. Using this drip to raise IOP above systolic arterial blood pressure, a practitioner temporarily halts inner retinal blood flow (ischemia). When circulation is reinstated (reperfusion) by removal of the cannula, severe cellular damage ensues, resulting ultimately in retinal neurodegeneration. Recent studies demonstrate inflammation, vascular permeability, and capillary degeneration as additional elements of this model. Compared to alternative retinal I/R methodologies, such as retinal arterial ligation, retinal I/R injury by elevated IOP offers advantages in its&#160;anatomical specificity, experimental tractability, and technical accessibility, presenting itself as a valuable tool for examining neuronal pathogenesis and therapy in the retinal neurovascular unit.

This article describes a procedure for inducing retinal ischemia-reperfusion injury by elevated intraocular pressure in mice. Retinal ischemia-reperfusion injury by elevated intraocular pressure serves to model human pathologies characterized by compromised oxygen and nutrient delivery in the retina, enabling researchers to examine potential cellular mechanisms and treatments for human diseases of the retinal neurovascular unit.

视网膜缺血再灌注损伤的小鼠模型通过眼压升高

Retinal ischemia-reperfusion (I/R) is a pathophysiological process contributing to cellular damage in multiple ocular conditions, including glaucoma, ...

Partial Optic Nerve Transection in Rats: A Model Established with a New Operative Approach to Assess Secondary Degeneration of Retinal Ganglion Cells

Previous studies have shown that the secondary degeneration of retinal ganglion cells (RGCs) occurs commonly in glaucoma. Partial optic nerve transection is considered a useful and reproducible model. Compared with other optic nerve injury models used commonly for assessing secondary degeneration, e.g. complete optic nerve transection and optic nerve crush models, the partial optic nerve transection model is superior as it distinguishes primary from secondary degeneration in situ. Therefore, it serves as an excellent tool for evaluating secondary degeneration. This study describes a novel operative approach of partial optic nerve transection by directly accessing the area of the retrobulbar optic nerve through the orbital lateral wall of the eyeball. Moreover, we present a newly designed, low cost surgical instrument to assist with transection. As demonstrated by the representative results in distinguishing the boundary of primary and secondary injury areas, the new approach and instrument ensures high efficiency and stability of the model by providing adequate space for surgical operation. This in turn makes it easy to separate the meningeal sheath and ophthalmic vessels from the optic nerve before transection. An additional benefit is that this space-saving operative approach improves the investigators&#39; ability to administer drugs, carriers, or selective RGC tracers to the stump of the partially transected optic nerve, allowing the exploration of mechanisms behind secondary injury in RGCs, in a new way.

Secondary degeneration of retinal ganglion cells (RGCs) occurs commonly in glaucoma. This study describes an innovative operative approach for partial optic nerve transection. The use of this space-saving operative approach extends the model's application range, and allows exploration of secondary injury mechanisms in RGCs in a new way.

大鼠部分视神经切断术: 建立一种新的手术方法评价视网膜神经节细胞二次变性的模型

Previous studies have shown that the secondary degeneration of retinal ganglion cells (RGCs) occurs commonly in glaucoma. Partial optic nerve transection ...

Oxygen-Induced Retinopathy Model for Ischemic Retinal Diseases in Rodents

One of the commonly used models for ischemic retinopathies is the oxygen-induced retinopathy (OIR) model. Here we describe detailed protocols for the OIR model induction and its readouts in both mice and rats. Retinal neovascularization is induced in OIR by exposing rodent pups either to hyperoxia (mice) or alternating levels of hyperoxia and hypoxia (rats). The primary readouts of these models are the size of neovascular (NV) and avascular (AVA) areas in the retina. This preclinical in vivo model can be used to evaluate the efficacy of potential anti-angiogenic drugs or to address the role of specific genes in the retinal angiogenesis by using genetically manipulated animals. The model has some strain and vendor specific variation in the OIR induction which should be taken into consideration when designing the experiments.

Oxygen-induced retinopathy (OIR) can be used to model ischemic retinal diseases such as retinopathy of prematurity and proliferative diabetic retinopathy and to serve as a model for proof-of-concept studies in evaluating antiangiogenic drugs for neovascular diseases. OIR induces robust and reproducible neovascularization in the retina that can be quantified.

罗登斯缺血性视网膜疾病的氧诱导视网膜病变模型

One of the commonly used models for ischemic retinopathies is the oxygen-induced retinopathy (OIR) model. Here we describe detailed protocols for the OIR ...

Full-Circle Cauterization of Limbal Vascular Plexus for Surgically Induced Glaucoma in Rodents

Glaucoma, the second leading cause of blindness worldwide, is a heterogeneous group of ocular disorders characterized by structural damage to the optic nerve and retinal ganglion cell (RGC) degeneration, resulting in visual dysfunction by interrupting the transmission of visual information from the eye to the brain. Elevated intraocular pressure is the most important risk factor; thus, several models of ocular hypertension have been developed in rodents by either genetic or experimental approaches to investigate the causes and effects of the disease. Among those, some limitations have been reported such as surgical invasiveness, inadequate functional assessment, requirement of extensive training, and highly variable extension of retinal damage. The present work characterizes a simple, low-cost, and efficient method to induce ocular hypertension in rodents, based on low-temperature, full-circle cauterization of the limbal vascular plexus, a major component of aqueous humor drainage. The new model provides a technically easy, noninvasive, and reproducible subacute ocular hypertension, associated with progressive RGC and optic nerve degeneration, and a unique post-operative clinical recovery rate that allows in vivo functional studies by both electrophysiological and behavioral methods.

The goal of this protocol is to characterize a novel model of glaucomatous neurodegeneration based on 360&#176; thermic cauterization of limbal vascular plexus, inducing subacute ocular hypertension.

角膜缘血管丛全圆烧灼治疗啮齿动物手术诱发的青光眼

Glaucoma, the second leading cause of blindness worldwide, is a heterogeneous group of ocular disorders characterized by structural damage to the optic ...

A Murine Model of Ischemic Retinal Injury Induced by Transient Bilateral Common Carotid Artery Occlusion

Diverse vascular diseases such as diabetic retinopathy, occlusion of retinal veins or arteries and ocular ischemic syndrome can lead to retinal ischemia. To investigate pathological mechanisms of retinal ischemia, relevant experimental models need to be developed. Anatomically, a main retinal blood supplying vessel is the ophthalmic artery (OpA) and OpA originates from the internal carotid artery of the common carotid artery (CCA). Thus, disruption of CCA could effectively cause retinal ischemia. Here, we established a mouse model of retinal ischemia by transient bilateral common carotid artery occlusion (tBCCAO) to tie the right CCA with 6-0 silk sutures and to occlude the left CCA transiently for 2 seconds via a clamp, and showed that tBCCAO could induce acute retinal ischemia leading to retinal dysfunction. The current method reduces reliance on surgical instruments by only using surgical needles and a clamp, shortens occlusion time to minimize unexpected animal death, which is often seen in mouse models of middle cerebral artery occlusion, and maintains reproducibility of common retinal ischemic findings. The model can be utilized to investigate the pathophysiology of ischemic retinopathies in mice and further can be used for in vivo drug screening.

Here, we describe a mouse model of retinal ischemia by transient bilateral common carotid artery occlusion using simple sutures and a clamp. This model can be useful for understanding the pathological mechanisms of retinal ischemia caused by cardiovascular abnormalities.

由瞬态双边常见胡萝卜动脉闭塞引起的缺血性视网膜损伤的 Murine 模型

Diverse vascular diseases such as diabetic retinopathy, occlusion of retinal veins or arteries and ocular ischemic syndrome can lead to retinal ischemia. ...