实验性高血压大鼠视网膜的的光电镜观察

应用光、电镜方法观察１２只正常大鼠视网膜，１２只实验性高压大鼠视网膜，结果表明：高血压大鼠视网膜毛细血管基膜增厚，管腔狭窄致视网膜缺血缺氧引起节细胞和视细胞外节的病变。多数节细胞水肿、胞浆淡染、线粒体空泡化、滑面内质网扩张、部份粗面内质网扩张、脱粒；甚至有少数节细胞胞膜破裂与邻近节细胞胞浆相融合。而视细胞的改变主要在于外节中膜盘凌乱，排列不整齐，特别是外节基底部新生的膜盘病变为甚。视网膜中的Ｍｕｉ     

亚低温对大鼠视网膜缺血再灌注自由基损伤的保护

目的 :探讨亚低温是否对大鼠视网膜缺血再灌注自由基损伤具有保护作用。方法 :采用提高眼压法造成视网膜缺血后 ,恢复眼压形成血流再灌注。应用透射电镜观察正常对照组、缺血再灌注组和亚低温缺血再灌注组三组大鼠视网膜的超微结构 ;同时测定三组大鼠视网膜组织超氧化物歧化酶 (SOD)活性和丙二醛 (MDA)的含量。结果 :缺血再灌注组大鼠视网膜视细胞外节膜盘肿胀 ,排列紊乱 ;节细胞水肿明显 ,多数线粒体肿胀 ;滑面内质网扩张 ,部分粗面内质网扩张、脱粒。亚低温缺血再灌注组视网膜的视细胞外节膜盘略见疏松 ;节细胞胞浆内可见肿胀线粒体 ,但肿胀较轻。缺血再灌注组和亚低温缺血再灌注组大鼠视网膜的SOD含量分别是 5 6 2± 1 .8nu/ml和72 .3± 2 .3nu/ml;MDA含量分别是 8.0 5 4+0 .893nmol/ml和 6.0 2 3 +0 .3 98nmol/ml。结论 :亚低温可通过抑制脂质过氧化反应和自由基的过多生成 ,对视网膜缺血再灌注损伤起保护作用。     

糖尿病大鼠视网膜视细胞超微结构病理变化的研究

目的:探讨糖尿病大鼠视网膜病变（diabetic retinopathy.DR.简称糖网病）,早期视细胞（视感受器）的超微结构病变,为糖网病光感受器功能障碍提供形态学依据。方法:选择清洁级SD大鼠随机分成正常对照组（CON）、糖尿病1月（DM1）、3月（DM3）和6月（DM6）。按60mg/kg腹腔内注射链脉佐菌素（STZ）诱导大鼠糖尿病,每组12只,取大鼠视网膜透射电镜观察。处死前每月测血糖和眼底镜检查1次。结果:病程1个月:视杆、视锥细胞的外节膜盘模糊不清,膜盘间隙略有扩大,椭圆体内中心粒和纤毛仍清晰可见,线粒体规则的排列在周围。病程3个月,视细胞外节膜盘间隙明显扩大,纵横交错,排列紊乱,并发生局灶性断裂,椭圆体内有部分线粒体肿胀、脱嵴。毛细血管扩张,神经纤维中心微管也有水肿。病程6个月:视细胞外节内膜盘断裂溃变,颜色淡,并出现许多泡沫状结构,椭圆体内的线粒体变小,排列不规则,有的脱嵴、水肿,毛细血管已有部分由扩张转为狭窄。结论:糖尿病早期毛细血管由局部扩张转为狭窄,视网膜因缺血、缺氧的加重导致视细胞超微结构的病理改变,并随病程的进展而加重。     

高血压大鼠视网膜溶酶体酶的电镜细胞化学研究

目的：探讨高血压大鼠视网膜溶体酶活性增强的原因及其在高血压大鼠视网膜病变中的作用。方法：应用电镜酶细胞化学方法对２０周龄正常京都种大鼠和同周龄的自发性高血压大鼠视网膜组织和胞嘧啶单核苷酸酶活性部位进行定位观察。结果：在正常大鼠视网膜组织中,胞嘧啶单核苷酸酶沉淀颗粒主要位于溶酶体内,色素上皮细胞含丰富的溶酶体,视细胞膜盘基部、外网层、内网层和节细胞中见到较多溶酶体,其它各层溶酶体较少,视细胞外节膜盘     

糖尿病早期大鼠视网膜视细胞超微结构改变与醛糖还原酶的相关性及氨基胍的保护作用

目的 :探讨糖尿病早期大鼠视网膜视细胞超微结构改变与醛糖还原酶 (Aldosereductase ,AR)含量变化的相关性及氨基胍 (Aminoguanidine,AG)的保护作用。方法 :选择健康成年雄性SD大鼠 ,随机分成正常对照组、糖尿病组和糖尿病AG治疗组。一次性腹腔注射链脲佐菌素 (Streptozotin ,STZ)诱发糖尿病模型 ,分别于第 3 0天和第 90天测定视网膜组织AR含量 ;并在第 90天时取视网膜行透射电镜观察视细胞超微结构。结果 :糖尿病早期大鼠视网膜AR含量随糖尿病时间的增长而增多 ;糖尿病 90天大鼠视网膜的视细胞外节膜盘排列紊乱 ,间隙扩大 ,内节线粒体水肿 ,有的空泡化 ;AG治疗组大鼠视网膜AR含量明显低于糖尿病未治疗组 ,糖尿病 90天大鼠视网膜视细胞外节膜盘少量排列紊乱 ,内节线粒体正常。结论 :糖尿病早期视网膜视细胞超微结构改变与AR含量变化有关 ,AG可通过抑制AR活性而保护视细胞     

开搏通,可乐宁对高血压大鼠视网膜病变疗效的超微结构观察

应用光，电镜观察高血压大鼠经开搏通和可乐宁终身治疗后，其视网膜超微结构变改善情况，结果表明：高血压大鼠视网膜超微结构的改变主要在视细胞外节，内节，神经节细胞的胞体和轴突，经开搏通终身治疗后视网膜超微结构病变得以改善，而经可乐宁治疗则无明显改变，为高血压患者的早期预防和防治提供重要参考。     

糖尿病早期大鼠视网膜毛细血管及视细胞超微结构变化规律

目的：探讨大糖尿病视网膜病变（糖网病）早期的视网膜毛细血管及视细胞的病变规律。材料与方法：选择健康成年Wistar大鼠,随机分成正常对照组,糖尿病1月,3月和6月组,一次性腹腔内注射链脲佐菌素STZ）诱导大鼠糖尿病,制备视网膜超薄切片,透镜观察并计算机图像分析。结果：病程1月,周细胞和内皮细胞核异染色质聚集靠边;视杆膜盘间隙略扩大。3月,毛细血管细胞异染色质聚集严重,基底膜增厚;膜盘间隙扩大明显,局灶性断裂,溶解。视杆细胞膜固缩,异染色质浓集,视杆内节线粒体肿胀,甚至空泡变性,病程6月,以上改变更加严重,毛细血管狭窄,变形,甚至闭塞。结论：糖网病早期大鼠视 膜毛细血管病变的同时,变出现视感受器超微结构的改变,随病程的进展病变逐渐加重。     

自发性高血压大鼠视网膜色素上皮超微结构

目的：观察高血压大鼠视网膜色素上皮的超微结构,探讨其与神经视网膜病变的关系。方法：用透射电镜观察５、６、７月龄自发性高血压大鼠及同月龄京都种大鼠视网膜色素上皮细胞超微结构,结果：高血压大鼠视网膜色素线粒体肿胀,内质网扩张,基底部皱褶减少,微绒毛变稀疏,色素颗粒减少,这些退行性改变随鼠龄增大血压的增高而加重。结论：Ｄ 谪血压视网膜病变的早期视网膜色素上皮细胞已有缺血、缺氧所致的退行性改变,提示早期的     

RCS大鼠视网膜感光细胞的凋亡

为研究遗传性视网膜变性中感光细胞组织结构的时程变化及调亡，对ＲＣＳ大鼠脑ＳＤ大鼠视网膜进行光镜观察和凋亡细胞ＴＵＮＥＬ检测。结果表明，与同龄ＳＤ大鼠相比，ＲＣＳ大鼠视网膜感光细胞从出生后１５ｄ开始，出现外节膜盘堆积；２０ｄ时，内节排列紊乱，消失，３０ｄ，细胞核固缩，细胞消失，到出生后６０ｄ，仅少许感光细胞保留；１００ｄ，几乎所有感光细胞消失。ＴＵＮＥＬ检测，从出生后２５ｄ开始，ＲＣＳ大鼠视网膜有Ｔ     

杞菊地黄汤防治MNU诱导大鼠视网膜变性的早期效应

目的:观察杞菊地黄汤在N-甲基-N-亚硝脲(MNU)诱导的SD大鼠视网膜变性早期的拮抗效应。 方法:生后46 d的雌性SD大鼠30只随机分为3组(n=10)：药物组以杞菊地黄汤灌胃，正常组和模型组以等量蒸馏水灌胃，每日1次，连续4 d。用药后第5 d，药物组和模型组大鼠皮下注射MNU 40 mg/kg，正常组皮下注射等量生理盐水做对照。注射后12 h，处死大鼠，每组大鼠的左眼（10眼）用于透射电镜观察；右眼（10眼）用于苏木素-伊红(hematoxylin eosin,HE)染色观察并测量分析视网膜全层及外核层厚度，部分眼球行TUNEL法染色并计算细胞凋亡百分率。 结果:光镜下各组大鼠视网膜组织学未见明显改变，视网膜全层及外核层厚度组间比较均无显著差异（P>0.05）。TUNEL法染色见模型组和药物组外核层存在细胞凋亡，正常组未见。电镜下正常组和药物组光感受器细胞大小和核染色质分布均匀；模型组光感受器细胞开始变小，核染色质开始浓缩, 外节膜盘疏松，膜型不完整。 结论:杞菊地黄汤通过抑制细胞凋亡等选择性拮抗MNU对大鼠视网膜光感受器细胞的早期损伤。     

Cellular and subcellular localization of heme oxygenase-2 in monkey retina

Carbon monoxide (CO), an activator of soluble guanylate cyclase (SGC) and generated enzymatically by heme oxygenases (HO), is considered to function as an intra- and intercellular neuromodulator or neurotransmitter in the central and peripheral nervous systems. HO-2 is the constitutive isoform of HO and is more prevalent in nervous tissues than in the other peripheral tissues. Because previous studies have demonstrated different distributions of HO-2 in the retina depending on the species of animals, the aim of this study was to identify which cell types of the monkey retina express HO-2. The expression of HO-2 protein was examined in monkey retina by Western blot analysis. Immunoblottings from monkey homogenates revealed a single clear protein band with a molecular mass of 36 kDa that is corresponding to rat HO-2. Immunoreactivity of HO-2 was found in the perikarya of ganglion cells. Density of immunoreactive ganglion cells was higher in the central area of retina than in the peripheral retina, and somata of larger ganglion cells were stained more densely than smaller ones. In electron microscopy, immunoreactivity of HO-2 was localized on the membrane of the endoplasmic reticulum and the nuclear outer membrane of the ganglion cells. By contrast, inner plexiform layer, inner nuclear layer and outer nuclear layer were devoid of HO-2 immunoreactivity. cGMP were strongly localized in all of ganglion cells. Some cells contributed to the relatively faint cGMP staining were seen in the inner nuclear layer. In combination of HO-2 and cGMP immunocytochemistry, the overlap of co-localization of HO-2 and cGMP would suggest that HO-2 in the ganglion cells would serve as a source for CO generation and CO could serve as a gaseous signaling molecule modulator of neural activity in the retina of monkey.     

Nogo-A在小鼠胚胎新生视网膜节细胞及其轴突的表达

目的 研究小鼠胚胎阶段Nogo-A在视网膜节细胞(RGCs)及其轴突上的表达及时程变化. 方法 取不同发育阶段的小鼠胚胎,采用免疫荧光染色,以激光扫描共焦显微镜观察Nogo-A在视觉传导通路中的表达.并采用免疫双标染色确定视网膜中表达Nogo-A蛋白的细胞类型. 结果 在视网膜发育的早期阶段(E12),Nogo-A密集表达于具有放射状形态的细胞上,Nogo-A免疫阳性产物出现在胞质、胞膜以及轴突上.Nogo-A与Tuj-1双标染色显示,此阶段的视网膜中几乎所有RGCs及其轴突都表达有Nogo-A;在稍晚的发育阶段(E13),视网膜中表达Nogo-A的RGCs数量明显减少,且仅出现在节细胞层以外的室周带和睫状体边缘区.在视网膜的神经纤维层,大部分RGCs轴突不再表达Nogo-A,仅有少量视觉纤维为Nogo-A免疫阳性;RGCs的神经发生基本完成后(E15), 视网膜中几乎检测不到Nogo-A免疫阳性的细胞,但视网膜纤维层仍有少量表达Nogo-A的节细胞轴突.与之类似,视神经盘、视茎、视交叉和视束都观察到少量Nogo-A免疫阳性的轴突.值得注意的是,视束中表达Nogo-A的纤维集中位于表浅部位,而此处恰为新近到达轴突的通过部位. 结论 Nogo-A在视网膜RGCs以及轴突上表达的时程变化和位置特点提示,新生RGCs及其轴突表达Nogo-A,成熟后RGCs内Nogo-A的表达则下调.推测新生RGCs及其轴突中表达的Nogo-A可能与减少轴突分叉等细胞的内在功能有关.     

Loss And Survival of Spiral Ganglion Neurons in the Guinea Pig After Intracochlear Perfusion with Aminoglycosides

Loss of cochlear hair cells results in a loss of ganglion cells and further neurodegenerative changes throughout the auditory pathway. Understanding more about the early stages of ganglion cell loss in vivo may lead to ways of ameliorating or preventing the loss of these neurons. To examine these stages, the effects of intracochlear perfusion with aminoglycoside antibiotics on the organ of Corti and spiral ganglion cells were evaluated in young adult guinea pigs at survival periods ranging from 1 hour to 12 weeks, using immunocytochemical and ultrastructural techniques. At 1 hour survival a base-to-apex gradient of damage was indicated in the cochlea by the appearance of severely damaged hair cells and injured ganglion cells in the basal coil while in the apical coil, hair cells were damaged but intact and ganglion cells appeared normal. By 4 hours the appearance of severely disrupted hair cells and damaged ganglion cells had extended throughout the cochlea. The ultrastructural appearance of many injured ganglion cells demonstrated features characteristic of cell death including condensed cytoplasm, non-marginal clumping of nuclear chromatin, and wrinkled nuclear membrane. Despite the loss of many ganglion cells, a population of these cells remained at 12 weeks survival. These contained large amounts of rough endoplasmic reticulum, were unmyelinated apart from the central process and were surrounded by satellite cells. These features are typical of ganglion cells during development, before the onset of hearing. Immunolabelling of cochlear whole mounts after hair cell destruction with protein gene product 9.5 (PGP 9.5) revealed the presence of neural elements in the organ of Corti at up to 12 weeks survival. These may associated with the remaining ganglion cells. In these surviving ganglion cells, the intense labelling with PGP 9.5 together with the increase in rough endoplasmic reticulum, indicates the presence of active protein synthesis which may be connected with their survival.     

Neurocircuitry of two types of neurotensin-containing amacrine cells in the turtle retina

The ultrastructural features and synaptic contacts of two types of neurotensin-containing amacrine cells in turtle retina were examined by electron immunocytochemistry, and the retinal peptides were characterized using radioimmunoassay and high-pressure liquid chromatography. The two types of cell were distinguished on the basis of their sizes, dendritic arborizations, synaptic connections and cytoplasmic staining characteristics. Type A cells had lightly labeled cytoplasm and large vertically elongated cell bodies which gave rise to a single primary process which in turn branched and ramified as smooth tapering processes in stratum 3 of the inner plexiform layer. Type A cells received approximately equal synaptic input from amacrine and bipolar cells. Type A amacrines had much more overall synaptic input than synaptic output, and they made conventional synaptic contacts onto bipolar, amacrine, and ganglion cells. Type B cells had a much darker-staining cytoplasm and a smaller cell body which gave rise to numerous delicate beaded dendrites which arborized in strata 3, 4 and 5 of the inner plexiform layer. Type B cells received primarily amacrine and some bipolar cell input. Type B cells had equal amounts of synaptic input and output and they made conventional synaptic contacts onto amacrine, bipolar, and ganglion cells. Whereas there were numerous large vesicles (120 nm diameter) that stained for neurotensin in both types of cells, conventional synaptic vesicles (60 nm diameter) were not labeled. In several cases these large labeled vesicles appeared to fuse with the cell membrane in non-synaptic regions and release their contents into extracellular space, which suggested a non-synaptic release of the neurotensin from type A neurons. Immunochemical and chromatographic studies demonstrated that the neurotensin-related material in retina was indistinguishable from neurotensin found in brain. These results are consistent with a neuroactive role for the neurotensin present within the large vesicles. The differences in the synaptic contacts and dendritic arborizations of the two amacrine cell types suggest they play distinctive functions in visual processing.     

Spatial and temporal correlation between early nerve fiber growth and neuroepithelial cell death in the chick embryo retina

Summary The distribution of cell death in the ventral pycnotic zone of the chick embryo retina was studied in Hamburger-Hamilton's stages 16 to 25 (2 1/2 to 4 1/2 days of incubation). The number of fragments appearing in the retina increases notably from stage 20 at which stage they are limited almost exclusively to the optic disc region. At the same time optic fibers are seen in this area for the first time. In stage 24 cell death phenomena are numerous in the ventral retina, and become even more extensive in the following stage. Stage 25 meanwhile sees a drop in cell death in the dorsal retina. The overall picture presented by cell remains and young ganglion cells indicates that in stages 19–23 cell death occurs mainly in the zone between the ganglion cells of the posterior pole and the optic stalk. In the stage 25 retina most of the cell fragments of the ventral retina are found on either side of the fissure, while ganglion cells in the process of sending out axons toward the fissure appear laterally (nasally and temporally) to these zones of degeneration. Hence a spatial and temporal correlation is established between fiber growth and neuroepithelial cell degeneration, allowing us to construct a hypothesis with regard to the role that cell death might play in setting up an initial pattern of optic fiber growth.     

Number, distribution and size of retinal ganglion cells in the jungle crow (Corvus macrorhynchos)

A retinal ganglion cell density map was generated using Nissl-stained retinal whole mounts from the jungle crow (Corvus macrorhynchos). The total number, distribution and size of these cells were determined in the area centralis, as well as in temporal, nasal, dorsal and ventral retinal regions. The mean total number of ganglion cells was estimated to be 3.6 x 10(6). The highest densities were found in the area centralis (25 600 /mm2) and the dorso-temporal part of the retina, suggesting the highest quality of vision. This density diminished nearly concentrically from the central area towards the retinal periphery. The number of ganglion cells was highest in the temporal retina followed, in order, by the nasal, dorsal and ventral retinal regions. Based on ganglion cell size, the retina seemed to consist of the following five regions: central, temporal, nasal, dorsal and ventral. Ganglion cell size ranged from 16 to 288 microm2, with smaller cells predominating in central regions above the optic disc and larger cells comprising more of the peripheral regions. The present study showed two highly populated areas of ganglion cells in the crow retina and it is expected that the crow retina provides well-developed monocular and binocular vision.     

Bifurcating retinal ganglion cell axons in the rat,demonstrated by retrograde double labelling

Summary By injecting two different tracers, one in each lateral geniculate nucleus, it was shown that some retinal ganglion cells project to both hemispheres in the rat. The double-labelled ganglion cells were confined to the temporal retina corresponding to the binocular visual field.     

Experimental retinal detachment causes widespread and multilayered degeneration in rabbit retina

Retinal detachment remains one of the most frequent causes of visual impairment in humans, even after ophthalmoscopically successful retinal reattachment. This study was aimed at monitoring (ultra-) structural alterations of retinae of rabbits after experimental detachment. A surgical procedure was used to produce local retinal detachments in rabbit eyes similar to the typical lesions in human patients. At various periods after detachment, the detached retinal area as well as neighbouring attached regions were studied by light and electron microscopy. In addition to the well-known degeneration of photoreceptor cells in the detached retina, the following progressive alterations were observed, (i) in both the detached and the attached regions, an incomplete but severe loss of ganglion cell axons occurs; (ii) there is considerable ganglion cell death, particularly in the detached area; (iii) even in the attached retina distant from the detachment, small adherent groups of photoreceptor cells degenerate; (iv) these photoreceptor cells degenerate in an atypical sequence, with severely destructed somata and inner segments but well-maintained outer segments; and (v) the severe loss of retinal neurons is not accompanied by any significant loss of Müller (glial) cells. It is noteworthy that the described progressive (and probably irreparable) retinal destructions occur also in the attached retina, and may account for visual impairment in strikingly large areas of the visual field, even after retinal reattachment.