依托咪酯对成年大鼠视网膜神经节细胞的差异性保护作用

目的 探讨依托咪酯对成年大鼠视神经损伤后视网膜不同部位视网膜神经节细胞（RGCs）存活的影响。方法 取55只成年雌性SD大鼠,于双侧上丘和顶盖前区及外侧膝状荧光金逆行标记RGCs,然后随机分为6组:正常组（n=5）,模型组（n=10）,脂肪乳组（n=10;视神经损伤后腹腔注射等体积脂肪乳,1次/d）,以及低、中、高剂量依托咪酯组（n=30;视神经损伤后腹腔注射依托咪酯,剂量分别为2、4、6 mg/kg,1次/d）。RGCs标记后5 d,距视神经根部1 mm处切断左侧视神经,7、14 d后采用视网膜平铺技术计数距视盘边缘1、2、3 mm处荧光金逆行标记的RGCs。结果 正常组距视盘边缘1、2、3 mm处RGCs密度分别为（2652±116）个/mm2、（2196±145）个/mm2、（1758±137）个/mm2,越靠近视盘,RGCs密度越高（P<0.05）;但是,模型组视神经损伤后7、14 d,距视盘边缘3 mm处RGCs存活率明显高于1、2 mm处RGCs存活率（P<0.05）。视神经损伤后7 d,低剂量依托咪酯显著增加距视盘边缘1 mm处RGCs存活率（P<0.05）,中、高剂量依托咪酯显著增加距视盘边缘1、2、3 mm处RGCs存活率（P<0.05）。视神经损伤后14 d,低剂量和中剂量依托咪酯对距视盘边缘1、2、3 mm处RGCs存活率均无明显影响（P>0.05）;高剂量依托咪酯明显增加距视盘边缘1 mm处RGCs存活率（P<0.05）。结论 大鼠RGCs在视网膜中分布是不均匀的,不同部位RGCs对视神经损伤反应不一样,对依托咪酯治疗敏感性也不一样;距视盘越近,对损伤反应越重,对依托咪酯治疗反应越敏感;依托咪酯剂量越高,对RGCs保护作用范围越广,作用持续时间越长。     

奥氮平与MECT治疗精神分裂症急性期攻击激越的对照研究

目的探讨奥氮平与改良电抽搐（modified ECT,MECT）治疗首次发作的精神分裂症患者急性期的疗效及安全性。方法前瞻性、开放性、随机对照设计,90例首次急性发作的精神分裂症患者随机分为三组：即奥氮平组,依托咪酯MECT组与丙泊酚MECT组,每组30例。奥氮平初始剂量为5mg/d,最大20mg/d;依托咪酯MECT组和丙泊酚MECT组分别为0.21~0.3mg/kg与1.82-2.44mg/kg诱导麻醉,MECT治疗隔日一次,两周共6次。治疗观察时间两周,治疗第1天及第14天以阳性与阴性症状量表（PANSS）的兴奋因子（EC）评定疗效。结果治疗两周后三组的PANSS-EC因子评分均显著下降,奥氮平组为（10.23±3.17）,依托咪酯MECT组为（9.04±2.48）,丙泊酚MECT组为（7.66±3.43）,三组之间差异无统计学意义（P〉0.05）。三组不良反应差异亦无统计学意义（P〉0.05）。结论奥氮平治疗精神分裂症急性期攻击激越症状的疗效,与依托咪酯或丙泊酚诱导的MECT相当。奥氮平是精神分裂症急性期攻击激越症状的有效治疗选择之一。     

神经干细胞移植对大鼠视神经损伤后节细胞的保护作用

目的探讨神经干细胞（NSCs）移植对视神经受损SD大鼠视网膜节细胞（RGCs）的保护作用。方法将48只健康成年SD大鼠随机分为N组（NSCs移植组）和C组（对照组），均使用精确校准方法在右眼造成部分视神经损伤，左眼作为正常对照。从胚胎SD大鼠海马分离NSCs。利用细胞培养和体内移植技术。将培养后的NSCs注入N组大鼠右眼玻璃体内，C组大鼠右眼玻璃体内注入同等体积的PBS。处死前3d在双上丘注射3％快蓝逆行标记双眼RGCs。将大鼠分别于注射NSCs或PBS后7d、14d、21d、28d处死，各分为4组。每组6只。分离视网膜置于荧光显微镜下，摄影输入计算机图像分析仪计数RGC。计算RGC标识率。另取6只健康成年SD大鼠作NSCs移植，分别于移植后7d、28d处死，每时间段3只。通过视网膜免疫荧光切片观察NSCs在视网膜的存活、整合情况。结果N组大鼠各时间段RGCs标识率与C组同时间段比较均增高，有显著性差异（P〈0．01）；N组与C组RGCs标识率均随时间延长而降低。且前后段时间比较有显著性差异，但N组降低速度明显慢于C组。NSCs移植7d后部分移植细胞迁移进入视网膜的内网层和节细胞层。28d后可见移植细胞广泛整合至宿主视网膜内。结论NSCs移植入视神经损伤大鼠视网膜后可提高视网膜神经节细胞的存活率．对受损的节细胞具有一定的保护作用。     

丙泊酚和依托咪酯在全麻诱导中对循环的影响

目的比较丙泊酚和依托咪酯乳剂在全麻诱导时对循环系统的影响。方法 40例择期妇科腹腔镜手术病人,ASAI~Ⅱ级,随机分为2组,A组（丙泊酚组）及B组（依托咪酯乳剂组）各20例,分别静脉注射丙泊酚2.0 mg/kg和依托咪酯乳剂0.2 mg/kg,监测仪测定诱导前、后的动脉血压和脉率。结果 A组病人麻醉诱导后SBP、DBP及HR较诱导前下降明显（P〈0.05）;B组病人麻醉诱导后各观察指标有不同程度下降,但与诱导前比较差异无统计学意义（P〉0.05）。结论与丙泊酚相比,依托咪酯乳剂在全麻诱导中对循环系统的影响更小。     

尼莫地平对急性损伤后大鼠背根节细胞c-fos、c-jun mRNA表达的影响

目的探讨钙离子拮抗剂尼莫地平对急性外周神经损伤后大鼠背根神经节c—fos、c-junmRNA表达的影响。方法建立大鼠坐骨神经切断模型，利用逆转录一聚合酶链反应（RT—PCR）半定量法，检测经尼莫地平预处理的大鼠在制模后不同时间（5min、15min、30min、60min、120min），以及同一时间（60min）应用不同剂量（2．5mg／kg、5mg／kg、10mg／kg）尼莫地平时大鼠背根神经节c—fos、c-junmRNA的表达水平的变化。结果与对照组比较，损伤组c-fos mRNA表达于损伤后30min、60min、120min，c-jun mRNA表达于损伤后15min、30min、60min、120min显著升高（均P〈0．05）；而尼莫地平组与对照组各时间点c—fos、c-jun mRNA表达比较差异无统计学意义。与损伤组比较，尼莫地平组c—los、c-jun mRNA表达于30min、60min、120min明显降低（均P〈0．001）。不同剂量尼莫地平预处理后，c—fos mRNA的表达随尼莫地平剂量的增加而逐渐减少，各剂量组问比较差异有统计学意义（均P〈0．05），c—fos mRNA表达水平与用药剂量呈负相关（r=-2．663，P〈0．05）；c-jun mRNA表达各剂量组问比较差异无统计学意义，亦无剂量相关性。结论急性外周神经损伤时应用钙离子拮抗剂尼莫地平，早期通过抑制c—fos、c-jun mRNA的表达，对外周神经损伤有一定的保护作用。     

吗替麦考酚酯对大鼠弥漫性轴索损伤后脑干胶质细胞激活及硫酸软骨素表达的影响简

目的探讨吗替麦考酚酯（MMF）对大鼠弥漫性轴索损伤（DAD后脑干胶质细胞激活及硫酸软骨素表达的影响。方法将72只DAI后SD大鼠随机分为3组：空白对照组、生理盐水治疗组（NS组）、吗替麦考酚酯治疗组（MMF组）。MMF组腹腔注射MMF（100mg／kg）干预;NS组腹腔注射等量生理盐水;空白对照组只作针扎刺激,不注射任何药物。伤后7、14、28d处死3组大鼠,取大鼠脑干进行巨噬细胞一小胶质细胞质抗原（ED-1）、胶质纤维酸性蛋白（GFAP）和硫酸软骨素（CS）免疫组化染色,检测活化小胶质细胞、活化星形胶质细胞、硫酸软骨素蛋白聚糖,并以累积光密度（IOD）值进行定量评估。结果在伤后不同时间点,MMF组活化小胶质细胞、活化星形胶质细胞、硫酸软骨素蛋白聚糖IOD值均显著低于NS组与空白对照组（P〈0．05）;而Ns组和空白对照组之间无统计学差异（P〉0．05）。结论MMF可抑制大鼠DAI后脑干小胶质细胞和星形胶质细胞激活,还可降低cs表达。     

依托咪酯预处理对大鼠局灶性脑缺血-再灌注损伤的保护作用

目的 探讨依托咪酯预处理对脑缺血-再灌注损伤的保护作用。方法 18只雄性SD大鼠,随机均分为3组,即脑缺血-再灌注组、依托咪酯预处理组、脂微球对照组。采用颈内动脉线栓栓塞致大脑中动脉阻塞模型,监测肛温及血糖,并于再灌注24h后断头处死动物,取大脑切片行2,3,5-氯化三苯基四氮唑染色,测量并计算脑梗死容积百分比。结果 依托咪酯预处理组脑梗死百分比明显低于脂微球对照组（P＜0.01）,低于缺血-再灌注组（P＜0.05）。但缺血-再灌注组与脂微球对照组相比差异无统计学意义。结论 依托咪酯预处理后可明显减小大鼠局灶性脑缺血-再灌注损伤后的脑梗死面积。     

利培酮对谷氨酸功能低下的精神分裂症小鼠模型的作用

目的 观察第二代抗精神病药利培酮对地卓西平马来酸盐（MK-801）所致谷氨酸功能低下精神分裂症小鼠模型的作用。方法 昆明种雄性小鼠122只。（1）取32只小鼠，分为溶媒（腹腔注射溶媒）和不同剂量利培酮（腹腔注射0．025，0．050，0．075mg／kg）4组，每组8只，观察利培酮对小鼠探究行为和自主活动的影响。（2）取50只小鼠分为5组，每组10只，分别为空白对照组（溶媒＋溶媒）、MK-801模型组（腹腔注射溶媒＋MK-801 0．25mg／kg）和3个不同剂量的利培酮（方法同前）组（3组均含0．25mg／kg的MK-801），观察利培酮对MK-801致小鼠自主活动增加的影响。（3）取40只小鼠分为5组，每组8只。给药方案同前，观察利培酮对MK-801引起的刻板行为的影响。结果 （1）与溶媒组比较，利培酮剂量为0．050mg／kg和0．075mg／kg时，小鼠的探究行为和自主活动总路程减少（均P〈0．05和（0．001）；但低剂量（0．025mg／kg）对小鼠的探究行为（P=0．093）和自主活动（P=0．263）的影响未达统计学意义。（2）利培酮（0．025-0．075mg／kg）呈剂量依赖性地抑制由MK801引起的自主活动增加和刻板行为（均P〈0．05）。结论 利培酮能特异性地抑制MK-801引起的行为改变。     

左乙拉西坦和托吡酯对癫(疒间)大鼠脑P-糖蛋白表达的影响

目的研究左乙拉西坦(LEV)和托吡酯(TPM)对癫大鼠脑P-糖蛋白(P-gp)表达的影响。方法将海人酸1.5μg(3μl)注射至SD大鼠海马制作癫模型(癫组),对照组大鼠海马注射3μl生理盐水(NS)。将癫组(18只)和对照组(15只)大鼠分别随机分为LEV、TPM和NS亚组(每亚组6只、5只),各亚组大鼠予相应药物(LEV50mg/kg、TPM40mg/kg、等体积NS)灌胃,每天1次,共30d。采用免疫组化EnVi-sion染色法检测大鼠颞叶、海马P-gp表达水平,采用LeicaQwin图像分析系统中平均整合灰度(MIB)值对P-gp表达水平进行半定量分析。结果癫各亚组大鼠颞叶和海马P-gp表达水平(MIB值)均显著高于其相应对照亚组(P<0.05～0.001);对照亚组中,LEV和TPM组与NS亚组间P-gp表达水平比较,差异无统计学意义;在癫组中,TPM亚组P-gp表达水平显著高于NS亚组(1550.3±371.9vs1049.7±282.8,P=0.004);而LEV亚组与NS亚组差异无统计学意义(1285.1±340.3vs1049.7±282.8,P=0.172)。结论癫发作可诱导...     

管内段视神经损伤后视网膜的形态学改变及GAP-43的表达

背景：视神经损伤后,视网膜发生一系列复杂的病理变化,从而造成功能丧失。 目的：观察管内段视神经损伤后视网膜的病理变化,比较视神经管减压术和激素对管内段视神经损伤的治疗作用。 设计、时间及地点：不同实验因素作用下视网膜病理形态学对比观察。实验于2008-09/11在潍坊医学院解剖学教研室完成。 材料：健康成年家兔36只,应用金属圆柱体自由落体冲击法建立兔右眼管内段视神经损伤模型。 方法：随机抽签法将实验兔分为单纯损伤组（n=24）,治疗组（n=12）。利用免疫组织化学、图像分析等技术,观察神经损伤后1、3、5、7、14 d及视神经管减压术、地塞米松、视神经管减压术＋地塞米松治疗14 d后,视网膜的形态学改变及GAP-43的表达。 主要观察指标：视神经损伤后RGCs记数及视网膜GAP-43表达阳性细胞记数的变化。 结果：纳入实验兔36只均进入结果分析。视神经损伤1 d后,RGCs平均记数轻度下降;损伤3、5、7 d时,RGCs数分别为对照组的84.48% 、72.23% 、57.46%;14 d时,节细胞仅有15.43％存活。损伤后3 d,视网膜切片中可见GAP-43表达阳性的细胞;伤后5 d阳性细胞增多;伤后7 d阳性细胞数和积分光密度值达最高峰;伤后14 d阳性细胞数下降。经手术减压、激素治疗、激素＋手术治疗后,RGCs存活率分别为36.01%、32.78%、56.98%。 结论：管内段视神经损伤后RGCs出现渐进性退变,数量逐渐减少;视神经管减压术和激素对管内段视神经损伤有一定的治疗作用,其疗效明显优于只采用一种方法。     

猫视神经慢性受压后视网膜神经节细胞的动态观察

目的 观察猫视神经慢性受压后视网膜神经节细胞(RGCs)的动态变化.方法 30只成年家猫按随机数字表法等分为正常对照组、假手术组、压迫1周组、压迫2周组、压迫4周组和压迫8周组,每组5只.利用球囊植入法建立慢性视神经损伤模型.所有动物在术前2周用Dil逆行标记RGCs.取各组动物视网膜进行光镜、电镜观察,并在荧光显微镜下对RGCs进行计数.结果 正常成年猫视网膜HE染色可见三层细胞核,各层间界限较为清楚,从玻璃体腔向巩膜依次为神经节细胞层、双极细胞层和感光细胞层;视神经慢性受压4周时视网膜变化仍不明显:受压8周时可见RGCs核明显稀疏,大而染色浅的细胞核基本消失,视网膜总厚度变薄,胶质细胞增生.电镜下正常猫RGCs核呈卵圆形、核大、核质均匀,有时可见核仁,胞浆占细胞比例小,但细胞器丰富;受压2周时视网膜无明显改变;受压4周和8周时可见RGCs胞浆成分疏松、内质网扩张、线粒体肿胀、质膜下出现空泡、核膜皱缩内陷、胞浆空化、染色质边聚.正常组DiI逆行标记的RGCs的密度在406～527个/mm2之间,平均为(465±38)个/mm2,中央区密度高于周边区;视神经受压后前4周RGCs数量无明显改变;受压8周时RGCs数量有显著下降,平均密度为(293±32)个/mm2.下降约37%.结论 视神经慢性受压后RCJCs将出现延迟的变性.为视神经受压后RGCs的保护提供了时机.     

电刺激对大鼠横断视神经视网膜节细胞的影响

目的在建立SD大鼠视神经横断和慢性电刺激模型的基础上,探讨电刺激对视网膜节细胞（RGCs）的保护作用。方法将大鼠随机分成电刺激治疗组和正常对照组,分离暴露右眼视神经并于球后1．5mm处进行横断。电刺激治疗组为分离横断视神经后给予电刺激,正常对照组为横断视神经后给予假性电刺激,在处死前2d断端处放人蘸有5％的荧光金（FG）的明胶海绵,以逆行标记RGCs。在3d、7d、14d不同的时间点处死动物并取材,进行HE染色并用荧光显微镜观察计数视网膜内存活的节细胞。结果在7d、14d电刺激治疗组存活的视网膜神经节细胞数目明显高于正常对照组,差异有显著意义（P〈0．05）。结论电刺激对视神经损伤有一定的保护作用。     

应用翼点入路构建猫急性视神经损伤动物模型

目的构建猫急性视神经压迫损伤动物模型。方法成年健康猫36只,按损伤时间分为6 h、1 d、3 d、7 d、14 d 5个组,每组6只,正常对照组6只。模仿临床上翼点入路,显微手术暴露视神经,以无创血管夹夹持视神经20 s,行视觉诱发电位检查并研究急性视神经损伤前后视觉电生理方面的变化。以上动物按不同时间分组处死后,取视神经、视网膜标本,进行光镜电镜分析,研究损伤后视神经、视网膜的病理改变。结果视神经损伤后观察动物瞳孔较正常瞳孔变大,行闪光视觉诱发电位（FVEP）检查,P1波潜伏期延长,振幅明显降低。电镜下可见损伤后的视神经神经内膜、髓鞘、各板层、轴膜及轴索结构紊乱,视网膜神经节细胞数目减少。结论急性视神经损伤后视神经髓鞘、视网膜发生病理学方面的改变,视觉诱发电位也随之变化。采用翼点入路构建的动物模型可用于急性视神经损伤的研究。     

Effect of NGF on the survival of rat retinal ganglion cells following optic nerve section

The ability of NGF (2.5S subunit) to support the survival of adult rat retinal ganglion cells (RGCs) and optic nerve fibers after intracranial section of the optic nerve was investigated. NGF was injected intraocularly at a dose of 3 micrograms/injection every 2.3 d from the day of axotomy to analysis. Control animals received cytochrome c injections. The survival of RGCs was analyzed in whole-mounted retinas after either cresyl violet staining or labeling with HRP applied to the proximal stump of the optic nerve. Survival times were 5 and 7 weeks. Diameter distribution and number of myelinated optic nerve fibers were assessed in ultrathin cross sections of the optic nerve. We found that RGCs surviving axotomy were much more numerous following NGF treatment compared with controls. Large-size cells were, in particular, preserved by NGF treatment. The quantitative ultrastructural studies indicated that the number of myelinated optic nerve fibers at 5 and 7 weeks postaxotomy was significantly greater in the NGF group with respect to the cytochrome c group. In agreement with the results obtained at the level of the RGCs, large-diameter axons were, in particular, preserved. We conclude that NGF injected intraocularly is effective in promoting the survival of RGCs and optic nerve fibers at least for a period as long as 7 weeks after intracranial section of the optic nerve.     

Pathological changes in the retina and growth associated protein-43 expression following treatment of intracanalicular optic nerve injury via optic canal decompression, dexamethasone or their combination

BACKGROUND: The main clinical treatments for optic nerve injury are optic canal decompression and systemic administration of hormones, but both treatments have disadvantages. OBJECTIVE: To observe the pathological changes in the retina and growth associated protein-43 (GAP-43) expression, to compare the treatment of optic canal decompression, hormones, and their combination with the intracanalicular optic nerve injury.DESIGN, TIME AND SETTING: A randomized, controlled animal study was performed at the Department of Anatomy, Weifang Medical University, China, from September 2007 to November 2008.MATERIALS: Dexamethasone (Shandong Huaxin Pharmaceutical, China) and rabbit anti-GAP-43 polyclonal antibody (Boster, China) were used.METHODS: All 36 healthy adult rabbits were randomly assigned to control group (n = 4), simple injury group (n = 20), and treatment group (n = 12). Intracanalicular optic nerve injury models were established using the metal cylinder free-fall impact method. The control group was left intact. The treatment group (four rabbits in each subgroup) was treated by optic nerve decompression, dexamethasone treatment (1 mg/kg daily via two intravenous infusions, 1/5 total dose reduction every 3 days, for 14 days), and simultaneously giving surgery and hormone treatment.MAIN OUTCOME MEASURES: Pathological changes in the retina were determined using hematoxylin-eosin staining. GAP-43 expression was detected using immunohistochemistry in the retina.RESULTS: Retina injury induced obvious pathological changes in the retina. With prolonged time after optic nerve injury, the number of retinal ganglion cells was gradually decreased, and reached the minimum on day 14 (P＜0.01). All three treatments increased the number of retinal ganglion cells (P＜0.01), but surgery + hormone treatment was most effective. No GAP-43 cells were present in the normal retinal, but they appeared 3 days after injury, peaked 7 days after injury, and then began to decline.CONCLUSION: Intracanalicular optic nerve injury induced obvious pathological changes in the retina, including increased GAP-43 expression. Optic canal decompression and hormones improved nerve repair after injury, and their combination produced better outcomes.     

Endothelin-1 impairs retrograde axonal transport and leads to axonal injury in rat optic nerve

The purpose of this study was to examine the effects of endothelin-1 (ET-1) on retrograde axonal transport in the rat optic nerve. Vehicle or ET-1 (0.2, 1, or 5 pmol/eye) were injected into the vitreous body in Sprague-Dawley rats. Retinal vessels were observed, using a fundus camera, before, and at 10 min, 3 days and 7 days after a single intravitreous injection. Two days after the injection, a neuronal tracer, fluoro gold, was administered via the superior colliculi to retrogradely label active retinal ganglion cells (RGCs). Five days after the tracer administration, retrogradely labeled RGCs were evaluated in the flat-mounted retina, and cross sections from each optic nerve were graded for injury by four independent, masked observers. ET-1 at 5 pmol/eye caused a significant constriction of retinal vessels (versus the vehicle-treated group) at 10 min after the injection. Intravitreous injection of ET-1 caused a dose-related decrease in the number of retrogradely labeled RGCs. Injection of 5 pmol/eye ET-1 led to a statistically significant decrease in the number of retrogradely labeled RGCs (versus the vehicle-treated group). ET-1 at 1 and 5 pmol/eye caused histological optic nerve damage (evaluated using a graded scale). The histological optic nerve damage correlated with the number of retrogradely labeled RGCs. In conclusion, a single intravitreous injection of ET-1 impaired retrograde axonal transport in the rat optic nerve and this impairment correlated with the histological optic nerve damage.     

Etomidate affects the anti-oxidant pathway to protect retinal ganglion cells after optic nerve transection

Our previous studies revealed that etomidate, a non-barbiturate intravenous anesthetic agent, has protective effects on retinal ganglion cells within 7 days after optic nerve transection. Whether this process is related to anti-oxidative stress is not clear. To reveal its mechanism, we established the optic nerve transection injury model by transecting 1 mm behind the left eyeball of adult male Sprague-Dawley rats. The rats received an intraperitoneal injection of etomidate(4 mg/kg) once per day for 7 days. The results showed that etomidate significantly enhanced the number of retinal ganglion cells retrogradely labeled with Fluorogold at 7 days after optic nerve transection. Etomidate also significantly reduced the levels of nitric oxide and malonaldehyde in the retina and increased the level of glutathione at 12 hours after optic nerve transection. Thus, etomidate can protect retinal ganglion cells after optic nerve transection in adult rats by activating an anti-oxidative stress response. The study was approved by the Animal Ethics Committee at Air Force Medical University, China(approval No. 20180305) on March 5, 2018.     

Immunohistochemical localization of CNTFRalpha in adult mouse retina and optic nerve following intraorbital nerve crush: evidence for the axonal loss of a trophic factor receptor after injury

Ciliary neurotrophic factor (CNTF) is important for the survival and outgrowth of retinal ganglion cells (RGCs) in vitro. However, in vivo adult RGCs fail to regenerate and subsequently die following axotomy, even though there are high levels of CNTF in the optic nerve. To address this discrepancy, we used immunohistochemistry to analyze the expression of CNTF receptor alpha (CNTFRalpha) in mouse retina and optic nerve following intraorbital nerve crush. In normal mice, RGC perikarya and axons were intensely labeled for CNTFRalpha. At 24 hours after crush, the immunoreactivity normally seen on axons in the nerve was lost near the lesion. This loss radiated from the crush site with time. At 2 days postlesion, labeled axons were not detected in the proximal nerve, and at 2 weeks were barely detectable in the retina. In the distal nerve, loss of axonal staining progressed to the optic chiasm by 7 days and remained undetectable at 2 weeks. Interfascicular glia in the normal optic nerve were faintly labeled, but by 24 hours after crush they became intensely labeled near the lesion. Double labeling showed these to be both astrocytes and oligodendrocytes. At 7 days postlesion, darkly labeled glia were seen throughout the optic nerve, but at 14 days labeling returned to normal. It is suggested that the loss of CNTFRalpha from axons renders RGCs unresponsive to CNTF, thereby contributing to regenerative failure and death, while its appearance on glia may promote glial scarring.