视网膜电图和多焦视网膜电图ON/OFF反应的研究进展

ON/OFF反应是人们从视网膜电生理反应中记录到的视网膜给光、撤光反应。它是通过不同的光感受器细胞形成不同的ON/OFF通路来完成。视网膜电图（ERG）和多焦视网膜电图（mf-ERG）ON/OFF反应的异常可明确提示ON/OFF通路及通路相关细胞的异常,在临床多种疾病,如先天性静止性夜盲,X连锁青年性视网膜病变等的诊断与治疗中有着重要意义。就ON/OFF通路（视锥ON/OFF通路,视杆ON/OFF通路,视杆慢快ON/OFF通路）和ERG、mfERGON/OFF反应的最佳记录方法、条件及在临床中的应用进行综述。     

兔眼脉络膜上腔多通道微电极阵列植入后视网膜电刺激阈值的研究

目的研究兔眼脉络膜上腔多通道微电极阵列芯片植入术后，电刺激视网膜诱发的中枢电诱发电位（EEP）的阈值。方法将多通道刺激电极（二氯代环二聚体为基底，铂电极）植入9只青紫蓝兔左眼后极部的脉络膜上腔，将铂丝制成的参比电极置于玻璃体腔，硬膜外放置记录电极。刺激电极采用双向刺激的方式发出电刺激，在中枢记录EEP。测量产生EEP的阈值，连续记录30次取其平均值。实验结束后处死动物取出眼球行组织学检查。应用检眼镜和OCT检查评价多通道微电极阵列芯片植入和清除后对兔眼组织的安全性。结果多通道微电极阵列芯片成功植入9只实验兔眼的脉络膜上腔。当脉络膜上腔刺激电极发出电刺激后，可以在硬脑膜外的记录电极处记录到EEP，阈值为（107．14±17．14）nC，（68．20±10．91）μC／cm。光学显微镜下显示视网膜结构完整，刺激电极附近无明显的组织结构的破坏。检眼镜及OCT检查显示相应的脉络膜组织与邻近组织间连接紧密。结论置于脉络膜上腔的电极发出的电刺激可以有效地诱发出EEP，且其阈值较低；脉络膜上腔是较理想的视网膜假体放置部位。     

小鼠视网膜胆碱能无长突细胞和方向选择性神经节细胞树突野发育的相关性研究

目的探讨小鼠视网膜方向选择性神经节细胞(DSGC)树突野(DF)的发育及其与胆碱能细胞阵列的关系。 方法选用中国科学院生物物理研究所实验动物中心繁殖的清洁级YFP(H)品系的转基因小鼠(种鼠来源于The Jackson实验室)共36只,0～1月龄,雌雄不限。对出生后不同发育时期(P8、P13及成年)的小鼠视网膜中ON/OFF DSGC及OFF DSGC的DF范围内包含的胆碱能细胞的数目采用单因素方差分析进行比较,当差异有统计学意义时,进一步两两比较。 结果ON/OFF DSGC作为经典的方向选择性神经节细胞,其树突具有两层树突结构,分别分布在视网膜内网状层的ON和OFF亚层中,其树突弯曲度和树突分支之间的夹角比较大,分支多向胞体方向返回呈半环状,显著的特点是同一细胞的树突不会发生交叉。P8时,D2亚类神经节细胞(即ON/OFF DSGC)DF范围中分别包含(25.6±4.8)个内核层(INL)的胆碱能无长突细胞和(28.4±5.7)个视网膜神经节细胞(GCL)的胆碱能无长突细胞(n＝7);P13时,D2亚类神经节细胞DF范围中分别包含(30.8±9.5)个INL的胆碱能无长突细胞和(35.2±10.4)个GCL的胆碱能无长突细胞(n＝10);成年时,D2亚类神经节细胞DF范围中分别包含(33.7±7.4)个INL的胆碱能无长突细胞和(32.1±5.6)个GCL的胆碱能无长突细胞(n＝9),三个时期的胆碱能无长突细胞的数目差异均无统计学意义(F＝2.16,1.55;P>0.05)。而视网膜中另外一种方向选择性神经节细胞OFF DSGC的DF范围内无长突细胞的数目从P8到P13先增多,然后从P13到成年又减少。P8时,该类细胞DF范围内位于GCL的无长突细胞数目为(20.0±2.5,n＝8)个,明显少于P13时的(32.0±7.1,n＝6)个;成年时,数目又减少到(23.7±7.5,n＝14)个。,三个时期的胆碱能无长突细胞的数目差异均无统计学意义(F＝6.19,1.55;P<0.05)。 结论小鼠视网膜ON/OFF DSGC的DF在出生后早期就已经发育成熟,并和胆碱能细胞形成稳定的联系,不再受后期双极细胞及光刺激的影响,而OFF DSGC的DF发育可能包含不同的分子和细胞机制。     

弱视治疗的新设想:闪烁刺激仪

功能性弱视的解剖——功能病变的特点是外侧膝状体神经元减少,病因机制的特点是两眼在外侧膝状体神经元水平不平衡,可能继发于双眼感觉输入的不同。人类和脊椎动物有3种神经节细胞,ON纤维,OFF和ON—OFF纤维,第一种在刺激开始时反应,第二种在刺激结束时反应,第三种对两种情况都有反应。以间断刺激可引起不同方式的反应:低频时,每个光刺激首先激发ON成分的反应,最后激发OFF成分的反应;频率较高时,ON—OFF成分反应,再增加频率,但未达到融合,则OFF成分先中止,     

视网膜电图和多焦视网膜电图视杆细胞ON和OFF反应记录研究

目的:研究全视野视网膜电图(electroretinogram,ERG)和多焦视网膜电图(multifocal eletroretinogram,mf-ERG)视杆细胞ON和OFF反应记录条件并分析其波形特征。方法:2例正常人放瞳、暗适应30 min后,分别采用矩形刺激(rectangle stimulus)、锯齿状的 rapid on和rapid off刺激模式记录反应波形,并改变刺激强度和频率观察波形变化。采用模拟矩形刺激、锯齿状的rapid on和rapid off刺激模式记录mf-ERG波形。结果:ERG采用矩形和rapid-on刺激模式可记录到大的正向波,随刺激频率增加,振幅减小, 潜伏时变化不明显。采用rapid-off刺激模式记录到小的负向波,潜伏时80 ms左右,在负向波下降支近波谷处可见小的正向波。随刺激频率增加,负向波潜伏时延长,而小正向波振幅逐渐减小。当刺激频率大于3 Hz时,上述反应均出现类似振荡电位波形。mf-ERG采用模拟矩形和模拟rapid-on刺激模式可记录到大的正向波,其波形特征与ERG矩形刺激模式的波形类似;采用模拟rapid-off刺激模式仍可记录大的正向波,但其后出现较大陡峭的负向波。结论:采用锯齿状的rapid-on和rapid-off刺激模式可以记录到视杆细胞ON和OFF反应,视杆细胞OFF反应的负向波下降支近波峰处存在小的正向波,采用模拟的rapid-on刺激模式记录到mf-ERG视杆细胞ON反应。建议记录ERG视杆细胞ON和OFF反应采用0．5-1Hz 刺激频率和低强度刺激光。将来可利用这些刺激模式研究视网膜疾病,具有一定的临床价值。     

人和小鼠视网膜双极细胞的形态及功能比较

目的比较人和小鼠视网膜视杆双极细胞形态和药物模拟对光反应的电流特性。方法实验研究。对视网膜冰冻切片行免疫荧光染色,用PKC-α抗体标记视网膜视杆双极细胞,以观察其形态分布特点。在灌流充氧的情况下制备视网膜薄片切片,行视网膜ON型以及OFF型双极细胞的全细胞膜片钳记录。分别在ON型双极细胞和OFF型双极细胞上给予快速加药40 µmol/L LY3414925或100 µmol/L AMPA,诱导出谷氨酸电流,以记录双极细胞模拟对光反应,并比较人和小鼠的谷氨酸电流动力学的差异,人和小鼠各项数据比较采用非参数检验（Mann-Whitney检验）进行处理。结果人和小鼠的视网膜视杆双极细胞形态分布相似,但PKC-α表达略有不同。膜片钳结果显示人视网膜ON型双极细胞的模拟对光反应的上升相的达峰时间为（1.91±0.11）ms,与小鼠视网膜ON型双极细胞[（0.83±0.08）ms]相比明显较长（U=0.00,P＜0.01）,而人视网膜ON型双极细胞的模拟对光反应恢复时间为（1.34±0.40）ms,明显短于小鼠[（20.06±3.07）ms]（U=0.00,P＜0.01）。但人和小鼠视网膜OFF型双极细胞电流动力学即电流幅度[人：（143.0±2.1）pA;小鼠：（136.3±2.2）pA]、反应上升时间[人：（1.91±0.35）ms;小鼠：（1.28±0.52）ms]和恢复时间[人：（220.5±10.8）ms;小鼠：（168.1±29.3）ms]差异均无统计学意义。结论 视杆双极细胞在人和小鼠视网膜中分布位置和形态大致相似。人和小鼠视网膜ON型双极细胞电流特性有差异。     

MNU诱导视网膜外层退行变性的细胞电生理和超微结构特征

目的：观察N-甲基-N-亚硝基脲（MNU）诱导的小鼠视网膜外层变性损伤的细胞电生理特征和超微结构变化。方法：实验研究。通过腹腔注射PBS和MNU,将C57/BL小鼠60 只随机分为对照组和MNU造模组。运用膜片钳电生理技术,观察位于外丛状层的双极细胞的电生理活动。用透射电子显微镜观察视网膜的超微结构。结果：膜片钳结果显示,给MNU后7 d,ON型双极细胞（ON-BC）对药物氨基（环丙基）（ 4-膦酰苯基）乙酸电生理反应完全消失,而OFF型双极细胞（OFF-BC）对药物α-氨基-3-羟基-5-甲基-4-异恶唑丙酸的刺激仍有电生理反应。给MNU后2 d,位于光感受器细胞外节（OS）的盘膜结构变薄。给MNU后5 d,OS消失,位于光感受器细胞内节（IS）的线粒体等细胞器严重肿胀。给MNU后10 d,IOS消失,光感受器细胞的核层变薄,核呈不同程度的浓染。下游的双极细胞核周间隙增宽,在双极细胞胞浆中有大量的自噬体。结论：MNU对ON型信号通路的损伤,比对OFF型信号通路的损伤要严重一些。MNU导致的视网膜损伤主要位于外侧（包括外核层和外丛状层）。MNU致光感受器细胞损伤的机制是凋亡。     

玻璃体腔注射促红细胞生成素对大鼠视网膜结构和功能的影响

促红细胞生成素（erythropoietin,EPO）对视网膜光损伤、视网膜缺血-再灌注损伤、高眼压视网膜神经节细胞损伤、视神经损伤诱导的神经节细胞损伤及视神经轴突再生、早期糖尿病视网膜病变视网膜神经元、血-视网膜屏障和变应性视神经脱髓鞘病变均具有保护作用。本研究将重组大鼠EPO注入大鼠玻璃体腔,旨在观察EPO对视网膜的结构和功能的影响以及是否会诱发视网膜新生血管形成。     

培养大鼠视网膜神经节细胞的形态学与电生理学特性

目的比较不同培养天数大鼠视网膜神经节细胞(retinal ganglion cells,RGCs)形态学特性与电生理功能,探讨其形态与功能的最佳培养时期。方法采用出生后0dLong Evans大鼠,取视网膜培养神经节细胞,分别于培养后第1d、4d、7d3个时间点观察细胞形态,并行膜片钳全细胞记录研究其静息膜电位(resting membrane potential,RMP)和动作电位(action potential,AP)的阈值、幅度及波宽。结果共记录到53个RGCs,根据AP类型RGCs分为单峰型(39个)、瞬变型(11个)和持续型(3个),其中以单峰型为主(占73.6%)。培养1d RGCs不易诱发AP,多数细胞需增加刺激强度后方可诱发出AP;培养4d时绝大多数RGCs给予20PA的刺激即可诱发出AP;培养7d时虽较容易诱发AP,但由于此时细胞存活状态较差,部分细胞(共记录28个细胞,其中8个不能诱发AP)给予不同强度的刺激,均不能诱发出AP。不同培养时期的RGCs静息膜电位和AP的特性无显著差异。结论随着培养时间的延长RGCs形态逐渐趋于成熟,但电生理功能仍处于幼稚状态;培养4d的RGCs形态和电生理状态最好。     

黄芩素与辅酶Q10对大鼠视网膜光损伤防护作用的研究

目的 观察黄芩素与辅酶Q10对实验性大鼠视网膜光损伤的防护作用。方法 SD大鼠通过24h持续光照射，建立视网膜光损伤模型。于光照前24h及光照前30min两次尾静脉注射给药。观察视网膜组织病理学改变及流式细胞术检测视网膜细胞凋亡率。结果 组织病理学结果显示，阳性对照组视网膜组织结构破坏严重，而黄芩素组、辅酶Q10组和联合用药组结构损伤明显减轻。流式细胞术检测结果，所有用药组视网膜细胞凋亡率明显低于阳性对照组（P〈0．05），联合用药组对细胞凋亡率的降低作用明显优于两药单独用药组（P〈0．05）。结论 黄芩素与辅酶Q10对视网膜光损伤诱发的细胞凋亡具有保护作用和明显的协同抗凋亡作用。     

Differential effects of charybdotoxin on the activity of retinal ganglion cells in the dark- and light-adapted mouse retina

Patch-clamp recordings were made from retinal ganglion cells in the mouse retina. Under dark adaptation, blockage of BK_Ca channels increases the spontaneous excitatory postsynaptic currents (EPSCs) and light-evoked On-EPSCs, while it decreases the light-evoked Off inhibitory postsynaptic currents (IPSCs). However, under light adaptation it decreases the light-evoked On-EPSCs, the spontaneous IPSCs and the light-evoked On- and Off-IPSCs. Blockage of BK_Ca channels significantly altered the outputs of RGCs by changing their light-evoked responses into a bursting pattern and increasing the light-evoked depolarization of the membrane potentials, while it did not significantly change the peak firing rates of light-evoked responses.     

Effects of the dopamine antagonist (+)-SCH 23390 on intracellularly recorded responses of ganglion cells in the rabbit retina.

The effects of the dopamine D1 antagonist (+)-SCH 23390 on the responses of ganglion cells in the superfused rabbit retinal preparation were studied by intracellular recording. At low micromolar concentrations, (+)-SCH 23390 hyperpolarized OFF-center brisk ganglion cells and reduced or abolished any spontaneous spike activity that was present. The light-evoked EPSPs at the onset of a spot or annulus were reduced or abolished, while the EPSPs at light offset were in most cases potentiated. (+)-SCH 23390 depolarized ON-center brisk ganglion cells and increased spontaneous spike activity. The light-evoked EPSPs to spots and annuli were either unaffected or reduced roughly to the same extent. The findings in this study are compared with findings in a recent study in which the effects of (+)-SCH 23390 on the extracellularly recorded responses of ganglion cells in the rabbit retina were examined.     

Analysis of second-order kernel response components of multifocal electroretinograms elicited from normal subjects

PURPOSE: It has been reported that the second-order kernel response components of multifocal electroretinograms (mERGs) reflect the electrical activity of the inner retinal layers. In this study, we have investigated whether the amplitudes of the second-order kernel response components correlate with the spatial distribution of human retinal ganglion cells. METHODS: Multifocal electroretinograms were recorded using the Veris III system from 5 healthy subjects with different stimulus and recording parameters. The mERGs were analyzed using the Veris Science software programs. The stimuli consisted of densely arranged arrays of 103, 61, 37 or 19 hexagonal elements. Four minutes were required to record one set of mERG responses using 8 sessions, and 8 minutes using 16 sessions. The second-order kernel response components were extracted and analyzed using the Veris Science program. RESULTS: The signal-to-noise ratio of the first-order kernel response components was improved considerably by the summation of the nine reproducible responses from the same subject but the second-order kernel response components were not. The summation of the nine reproducible responses was insufficient to identify an array of the second-order kernel response components. Both the first- and second-order kernel response components were larger when fewer hexagonal elements were used. There was no significant difference in the individual responses between the 4-minute and the 8-minute recordings. A response density analysis revealed a weak correlation between the amplitude distribution of the second-order kernel response components and the spatial distribution of human retinal ganglion cells. CONCLUSIONS: The distribution of the amplitudes of the second-order kernel response components of the mERGs elicited from normal subjects did not correlate with the distribution of human ganglion cells. This suggests that the theory that second-order kernel response components arise from the activity of retinal ganglion cells should be reconsidered.     

The sensitivity of light-evoked responses of retinal ganglion cells is decreased in nitric oxide synthase gene knockout mice

We have shown previously that increasing the production of nitric oxide (NO) results in a dampening of visual responses of retinal ganglion cells (G. Y. Wang, L. C. Liets, & L. M. Chalupa, 2003). To gain further insights into the role of NO in retinal function, we made whole-cell patch clamp recordings from ganglion cells of neural type nitric oxide synthase (nNOS) gene knockout mice. Here we show that in the dark-adapted state, the sensitivity of retinal ganglion cell to light stimulation is decreased in nNOS knockout animals. The lowest light intensities required to evoke optimal responses and the average intensities that evoked half-maximal responses were significantly higher in nNOS knockouts than in normal mice. Retinal histology and other features of light-evoked responses of ganglion cells in nNOS mice appeared to be indistinguishable from those of normal mice. Collectively, these results, in conjunction with our previous work, provide evidence that increasing levels of NO dampen visual responses of ganglion cells, while a lack of nNOS decreases the sensitivity of these neurons to light. Thus, NO levels in the retina are capable of modulating the information that ganglion cells convey to the visual centers of the brain.     

Spatiotemporal aspects of pulsed electrical stimuli on the responses of rabbit retinal ganglion cells

Implanted intraocular microelectrode arrays are being used to provide sight to individuals who are blind due to photoreceptor degeneration. It is envisioned that this retinal prosthesis will create the illusion of motion by stimulating focal areas of the retina in a sequential fashion through neighboring electrodes, much like the rapid succession of still images in movies and computer animation gives rise to apparent motion. Using a high-density microelectrode array, we examined the extracellularly recorded responses of rabbit retinal ganglion cells to a bar-shaped electrode array that was stepped at 50 μm increments at different rates across the retina and compared these respons2es to the responses generated to a similarly shaped light stimulus that was stepped across the retina. When the retina was stimulated at 1 step/s, retinal ganglion cells gave robust bursts of action potentials to both the electrode array and the light stimulus. The responses to the ‘moving’ electrode array decreased progressively with increasing stepping frequency. At 16 steps/s (highest frequency tested), the number of spikes per sweep and the number of bursts per sweep were reduced 75% and 67% respectively. In contrast, when the retina was stimulated at 16 steps/s with the ‘moving’ light stimulus, the number of spikes per sweep and the number of bursts per sweep were reduced only 43% and 25% respectively. These findings suggest that simple translation of object motion to sequential stimulation through neighboring electrodes may not be the best way to convey the perception of object motion in a patient with a retinal prosthesis.     

Activation of retinal ganglion cells in wild-type and rd1 mice through electrical stimulation of the retinal neural network

We compared the thresholds and response properties of extracellularly recorded retinal ganglion cells (RGCs) in wild-type and rd1 mouse retinas to electrical stimulation of the retinal neural network. Retinas were stimulated in vitro with biphasic current pulses (1 ms/phase) applied with a 400-microm diameter, subretinal electrode. Three types of responses were observed in both wild-type and rd1 RGCs. Type I cells elicited a single burst of spikes within 20 ms following application of the electrical stimulus, type II cells elicited a single burst of spikes with a latency greater than 37 ms, and type III cells elicited two and occasionally three bursts of spikes. For all ages examined, ranging from postnatal day (P) 25 to P186, the thresholds of RGCs were overall consistently higher in rd1 mice. Median threshold values were 14 and 50 muA in wild-type and rd1 mice, respectively. We propose that photoreceptors lower the thresholds for activation of RGCs whereas postreceptoral neurons determine the response properties of RGCs to electrical stimuli.     

αB-晶体蛋白对急性高眼压大鼠视网膜神经节细胞轴突再生作用的研究

目的:研究αB-晶体蛋白对大鼠急性高眼压后视网膜组织中αB-晶体蛋白含量,视网膜神经节细胞(retinal ganglioncells,RGCs)中生长相关蛋白-43(growth associated protein-43,GAP-43)表达和全视野视网膜电流图(full-field ERG,F-ERG)的b波振幅差异,探讨αB-晶体蛋白对急性高眼压后RGCs轴突再生的影响。方法:采用随机分组设计的实验研究。本实验选择120只健康、无眼疾SD大鼠,随机分为以下4组:αB晶体蛋白组(αB)30只,生理盐水组(S)30只,假手术组(P)30只,急性高眼压组(H)30只,均以右眼为实验眼,分别于术后7d和14d各取5只术眼的视网膜,行Western-blot法,观察急性高眼压后视网膜中αB-晶体蛋白的表达;术后7,14,21d各取5只术眼的视网膜,行免疫组织化学法,观察急性高眼压后RGCs的GAP-43表达;术前和术后1mo时应用全视野ERG的b波振幅变化测定视网膜功能。组间数据比较采用单因素方差分析(One-wayANOVA),组间两两比较采用SNK-q检验。结果:αB组视网膜中αB-晶体蛋白的表达于术后7d较高,14d时表达减弱(P=0.000),但同一时间点明显高于其他三组(P=0.006,P=0.024,P=0.007;P=0.006,P=0.008,P=0.010);αB组RGCs的GAP-43表达于术后7d达高峰,14d时表达减弱,21d时仍有少量表达(P=0.000),但各时间点明显高于其他三组(P=0.001,P=0.002,P=0.001;P=0.015,P=0.002,P=0.006;P=0.005,P=0.003,P=0.005);ERG-b波振幅于术后1mo较低(P=0.014,P=0.004,P=0.003,P=0.006),其中术前各组ERG-b波振幅无明显差异(P=0.993),术后1mo时αB组ERG-b波振幅明显高于其他三组(P=0.000,P=0.004,P=0.002)。结论:外源性αB-晶体蛋白能够提高视网膜αB-晶体蛋白的表达;αB-晶体蛋白通过促进RGCs中GAP-43的表达,从而促进RGCs的轴突再生;αB-晶体蛋白可促进视网膜功能的恢复,对大鼠视网膜无毒性作用。     

Thresholds for activation of rabbit retinal ganglion cells with a subretinal electrode

The ultimate success of a retinal prosthesis to create vision will likely depend upon developing a base of knowledge of how best to electrically stimulate the retina. Previously, we studied the responses of rabbit retinal ganglion cells (RGCs) to current pulses applied with an electrode placed on the epiretinal surface. In the present study, we examined the responses of rabbit RGCs to current pulses applied with a subretinal electrode. Single-unit extracellular recordings were made from OFF RGCs and ON RGCs in isolated retinas, which were stimulated with monophasic current pulses (0.1-50ms in duration), delivered through a 500-mum diameter electrode. All RGCs elicited one or more bursts of action potentials upon electrical stimulation of the retina. The timing of the bursts depended upon both the polarity of the electrical stimulus and the RGC type. With near-threshold current pulses, the response latencies of OFF RGCs to anodal stimulation were comparable to those of ON RGCs to cathodal stimulation, whereas the response latencies of OFF RGCs to cathodal stimulation were comparable to those of ON RGCs to anodal stimulation. Threshold currents for activation of RGCs decreased with increased pulse duration. For OFF RGCs, threshold currents for cathodal current pulses were, on average, 2-7.5 times higher (depending upon pulse duration) than the threshold currents for anodal current pulses. For ON RGCs, threshold currents for cathodal and anodal current pulses were, on average, nearly identical for all pulse durations and were equivalent to threshold currents of OFF RGCs to anodal stimulation. With respect to a subretinal prosthesis, our findings suggest the possibility that cathodal current pulses may bias activation of ON RGCs in blind patients.     

睫状神经营养因子对大鼠急性高眼压眼视网膜神经节细胞的保护作用

背景 青光眼可以引起视网膜神经节细胞(RGCs)凋亡,据报道睫状神经营养因子(CNTF)对外伤性视神经损伤有修复作用,其是否对青光眼视神经病变有保护作用尚少见报道. 目的 观察CNTF对大鼠急性高眼压眼RGCs的保护作用.方法 24只Wistar大鼠双眼采用眼前房平衡盐液加压灌注法建立大鼠急性高眼压模型,造模前2d左眼玻璃体内注入0.5μg CNTF 5μl,右眼以同样的方法注射磷酸钠溶液5μl,另取3只正常大鼠作为正常对照.造模后1、3、7、14 d过量麻醉法处死动物并摘除眼球,制备视网膜组织学切片后采用苏木精-伊红染色法进行形态学观察,光学显微镜下计数RGCs数目;采用免疫组织化学染色法观察RGCs层谷氨酸的表达情况.结果 正常对照组大鼠视网膜各层排列整齐,细胞边界清晰;模型对照组大鼠RGCs细胞膜、细胞核均发现异常改变,有细胞空泡样变;CNTF治疗组大鼠造模后变性的RGCs数量少.与模型对照组比较,造模后3、7、14 d CNTF治疗组RGCs数目明显增加,差异均有统计学意义(均P=0.000).免疫组织化学染色表明,造模后3～7d,CNTF治疗组RGCs层谷氨酸阳性细胞数分别为(5.50±1.04)个／3个高倍视野和(6.00±1.41) 个/3个高倍视野,明显低于模型对照组的(9.00±2.91)个／3个高倍视野和(10.83±1.94)个／3个高倍视野,差异均有统计学意义(均P=0.000),而造模后1d和14 d两组间谷氨酸阳性细胞数的差异均无统计学意义(P=0.578、0.180).结论 CNTF能够下调急性高眼压眼谷氨酸在RGCs中的表达,从而对RGCs提供保护作用.