PC12细胞缺氧后细胞凋亡与DNA损伤相关基因表达关系的研究

目的 探讨PC12细胞缺氧后细胞凋亡与DNA损伤的关系。方法 采用TUNEL法,结合应用流式细胞术观察PC12细胞缺氧培养不同时间点细胞凋亡现象,以及DNA损伤相关基因表达的改变。结果 在缺氧0.5h开始出现凋亡细胞,引时P53、P21^waf1/cip1蛋白表达开始增高。至缺氧1h凋亡细胞达高峰,此时P53、P21蛋白表达最高（P＜0.05）。至缺氧6－12h,则以坏死为主,此时以上基因表达均减弱。结论 PC12细胞在缺氧早期（0.5-2h）主要出现以凋亡为主的细胞死亡,伴有DNA损伤相关基因表达的动脉改变,提示缺氧后PC12细胞凋亡部分是由于DNA损伤严重、损伤不能及时修复所致。     

PC12细胞化学缺氧复氧损伤与缺氧诱导因子1表达的关系

目的 研究缺氧诱导因子1(HIF1)在PC12细胞化学缺氧复氧损伤中的作用。方法 在培养液中加入和去除氯化钴模拟化学缺氧和复氧，以乳酸脱氢酶(LDH)漏出和细胞超微结构改变作为细胞损伤指标，观察化学缺氧和复氧后不同时间细胞损伤和HIF1 α蛋白变化。结果 在氯化钴模拟化学缺氧实验中，LDH漏出明显增加，8h达高峰，随后逐渐下降，电镜结果与LDH改变相一致，HIF1 α蛋白表达在化学缺氧后2，4，8和12h均明显增加，8h达高峰，提示化学缺氧8h后细胞损伤逐渐减轻可能与HIF1 α蛋白水平升高有关。在模拟复氧实验中，LDH和细胞形态学改变都显示化学复氧8h细胞损伤最为严重，而HIF1 α蛋白表达在化学复氧4和8h均明显下降，提示细胞化学复氧损伤可能与HIF1 α蛋白水平下降有关。结论 HIF1对神经细胞化学缺氧复氧损伤具有保护作用。     

促红细胞生成素对新生大鼠皮质神经元体外缺氧缺糖损伤的保护作用研究

目的研究rhEPO对新生大鼠皮质神经元氧糖剥夺(OGD)损伤的保护作用及rhEPO的作用剂量及作用时间。方法新生Wistar大鼠皮质神经元原代培养7 d~11 d,随机分为正常对照组、OGD损伤组和rhEPO处理组。(1)建立皮质神经元的OGD模型,给予不同剂量的rhEPO(0.1、1、10、100 U/ml);(2)在不同时间(OGD损伤后0 h、24 h、48 h)给予10 U/ml rhEPO。观察各组细胞形态学改变,MTT法检测细胞存活率。结果与OGD损伤组比较,rh EPO(0.1、1、10 U/ml)处理可增加OGD损伤的皮质神经元的存活率(P0.05),且浓度为10 U/ml时rhEPO保护作用最强(P0.05)。皮质神经元OGD损伤后立即加入rhEPO(10 U/ml)保护作用最强(P0.05),损伤后24 h及48 h给药没有增加皮质神经元存活率。结论 rhEPO对体外缺氧缺糖损伤的大鼠皮质神经元具有保护作用,rhEPO有效浓度为0.1~10 U/ml,且其浓度为10 U/ml时保护作用最强;rhEPO在神经元损伤后立即给药保护作用最强。     

半夏总生物碱对6-OHDA诱导PC12细胞损伤的保护作用及机制

目的探讨半夏总生物碱(TAPT)对6羟基多巴胺(6-OHDA)诱导的大鼠肾上腺嗜铬细胞瘤细胞PC12细胞株损伤的保护作用及其机制。方法通过不同剂量TAPT预处理PC12细胞后,加入6-OHDA诱导氧化应激损伤。采用甲基噻唑基四唑比色法(MTT法)检测PC12细胞活力、天冬氨酸特异性半胱氨酸蛋白酶3(caspase-3)活性检测试剂盒测定caspase-3活性、黄嘌呤氧化酶法检测细胞总超氧化物歧化酶(T-SOD)活力,硫代巴比妥法检测丙二醛(MDA)的含量、按Fenton反应原理检测抑制羟自由基(·OH)的能力。结果浓度为100μmol/L的6-OHDA作用PC12细胞24h后,与正常对照组相比,细胞活力明显降低(P<0.05),T-SOD活性和抑制·OH的能力明显下降(P<0.05),而MDA含量和caspase-3活性明显升高(P<0.05);与6-OHDA组相比,TAPT处理组的PC12细胞活力逐渐升高(P<0.05),T-SOD活性和抑制·OH的能力明显上升(P<0.05),而MDA含量和caspase-3活性明显降低(P<0.05)。结论 TAPT对6-OHDA诱导的PC12细胞损伤具有一定的保护作用;提高T-SOD活性和抑制·OH的能力及降低MDA含量和caspase-3活性可能是其作用机制之一。     

低温对大鼠海马脑片缺氧无糖损伤的保护作用及其机制

目的利用离体海马脑片孵育液和电生理学技术研究低温对脑缺氧/无糖损伤的保护作用及其机制.方法 (1)观察大鼠海马脑片在缺氧/无糖条件下顺向群峰电位(orthodromic population spike,OPS)的变化及温度对它的影响;(2)用高效液相(high-performance liquid chromatography,HPLC)荧光法检测温度对缺氧/无糖导致的海马细胞外兴奋性/抑制性氨基酸(excitabilitory and inhibitory amino acid,EAA/IAA)水平变化的影响.结果 (1)37℃组海马脑片缺氧/无糖时缺氧损伤电位(hypoxic injury potential,HIP)出现率为87.5%(7/8),复氧/供糖1h后OPS恢复率为12.5%(1/8).低温组(32℃、25℃)OPS消失时间和HIP出现时间明显减少(P<0.01),复氧/供糖1h后OPS恢复程度(41%±34%、79%±33%)与37℃组(7.5%±21.2%)比较有显著性差异(P<0.05),而这3项指标25℃优于32℃;(2)37 ℃组缺氧/无糖时,EAA和IAA比对照组均显著增加(P<0.01),兴奋性毒性指数(excitory toxicity index,ETI)显著上升(P<0.01).复氧后各氨基酸水平均有所下降.而低温组缺氧/无糖导致的谷氨酸(Glu)、天门冬氨酸(Asp)和甘氨酸(Gly)升高显著减少(P<0.01),GABA却随着复氧时间的延长逐渐增加(P<0.01),ETI明显降低(P<0.01).这种效应25℃优于32℃.结论低温有明显的抗海马脑片缺氧/无糖损伤作用,其作用机制可能与低温维持了EAA和IAA的动态平衡,降低了EAA的兴奋性毒性作用有关.而其作用又以25℃优于32℃.     

P^38激酶在PC12细胞缺氧／再给氧损伤中的作用

目的：探讨ＰＣ１２细胞缺氧／再给氧损伤的信号转导机理。方法：培养的ＰＣ１２细胞先缺氧（９５％Ｎ２／５％ＣＯ２）６ｈ,然后重新给氧,预测不同时间点细胞的存活率和ｃａｓｐａｓｅ－３的活性;用ＭＴＴ法测存活率,ｃａｓｐａｓｅ－３检测试剂盒测ｃａｓｐａｓｅ－３活性。用ｐ３８拮抗剂ＳＢ２０３５８０孵育细胞２ｈ,之后缺氧／再给氧,观察ＳＢ２０３５８０对细胞存活率和ｃａｓｐａｓｅ－３活性的影响。结果：ＰＣ１２细胞缺氧／再给氧后ｃａｓｐａｓｅ－３活性的影响。结果：ＰＣ１２细胞缺氧／再给氧后ｃａｓｐａｓｅ－３活性明显增加并使细胞存活率下降,ＳＢ２０３５８０明显降低缺氧／复氧后ｃａｓｐａｓｅ－３的活性并使细胞死亡减少。结论：ＰＣ１２细胞缺氧／再给氧后至少可以通过激活ｐ３８、ｃａｓｐａｓｅ－３信号分子诱导ＰＣ１２细胞死亡。     

大黄素甲醚对PC12细胞缺氧损伤的保护作用

目的探讨大黄素甲醚对PC12细胞缺氧损伤的影响。方法体外培养PC12细胞,缺氧处理后给予小同溶浓度大黄素甲醚下预;四甲基偶氮唑盐（MTT）法检测PCI2细胞增殖活性的变化,油镜观察PC12细胞核形态变化,测定上清液中超氧化物歧化酶（SOD）含量,PCR分析丝裂原活化蛋白激酶p38（p38MAPK）和半胱氨酸蛋白酶-3（Caspase-3）的表达。结果缺氧24h后,大黄素甲醚干预后细胞核形态较清楚,偶有肿胀皱缩,少见颗粒样物质形成;大黄素甲醚干预后细胞活性明显增加（P〈0．05）;大黄素甲醚显著增加上清液中SOD含量（P〈0．05）。缺氧12h后PCR结果分析显示,大黄素甲醚显著降低p38MAPK和Caspase-3mRNA表达量（P〈0．01）。结论大黄素甲醚能增强缺氧所致神经元抗损伤能力,对神经元起保护作用。     

脑细胞缺氧损伤的发生发展及其防治对策

目前，一般认为脑缺氧引起神经元损伤是由于细胞外兴奋性氨基酸(EAA)，特别是谷氨酸(Glu)大量释放和堆积引起Ca^ 内流，使细胞内游离钙超载，对神经元产生损伤作用所致。但在EAA大量堆积之前发生了哪些病理生理反应，尚不清楚。近来有关研究表明，缺氧早期在Glu大量释放之前由于氧供不足，能量代谢障碍，细胞pH降低，     

Humanin通过保护线粒体功能对缺氧诱导的神经元损伤发挥保护作用

BACKGROUND： Humanin is a 24-amino acid peptide isolated from the brain of an Alzheimer’s disease patient. Several studies have indicated that Humanin can protect cells against cytotoxicity induced by various insults.
OBJECTIVE： To investigate the protective role of Humanin on hypoxia-induced neuronal death, and to determine the most appropriate therapeutic concentration of Humanin.
DESIGN, TIME AND SETTING： Neuropathophysiological, randomized, controlled experiment, conducted at the Department of Physiology and Neurobiology, Shanxi Medical University, between March 2007 and October 2007.
MATERIALS： Newborn Wistar rats, 5,5＇,6,6＇ tetrachloro-1,1＇,3,3＇-tetraethyl- benzimidazolylcarbo- cyanine iodide （JC-1, USA）, calcein-acetoxymethylester （calcein-AM, USA）, and Humanin （Shanghai, China） were used in this study. METHODS： Primary cortical neurons were cultured with dulbecco＇s modified eagle＇s medium containing 15% fetal bovine serum. Cultures were divided into three groups： control, hypoxia, and hypoxia ＋ Humanin. Various concentrations of Humanin （1, 10, and 20 μmol/L） were added to the cultures 16 hours prior to hypoxia induction. For hypoxic conditions, cells were maintained at 37 ℃ within an incubator chamber filled with 95% N2 and 5% CO2 for 24 hours. Cells in the control group were cultured in normal oxygen.
MAIN OUTCOME MEASURES： Cell viability was determined through the use of the vital dye calcein-AM, and the number of live cells was determined. Mitochondrial membrane potential （△Ψm） was assessed using the fluorescent probe JC-1. Mitochondrial permeability transition pore （mPTP） opening was determined with calcein-AM in the presence of cobalt chloride.
RESULTS： （1） Cell viability： Hypoxia for 24 hours induced death in a large number of neurons. Pre- treatment with 10 μmol/L and 20 μmol/L Humanin, 16 hours prior to hypoxia, protected cells against hypoxia. However, 1 μmol/L Humanin provided little protection. （2） △Ψm： △Ψm was re-duced after 24-hour hypoxia, as assessed by JC-1 and a confocal microscope. Pretreatment with 20 μmol/L Humanin preserved the loss of △Ψm. （3） mPTP： Hypoxia induced the opening of mPTP. Pretreatment with 20 μmol/L Humanin repressed the opening of mPTP, as most of the calcein fluorescence remained in the mitochondria.
CONCLUSION： Humanin （20 μmol/L） protects neuronal cells from hypoxia-induced insults by in- hibiting the opening of mPTP and preserving △Ψm.     

香芹酚对大鼠急性脊髓损伤的保护作用

目的 探讨香芹酚对大鼠脊髓损伤（SCI）后神经功能的影响及其机制。方法 将60只雄性SD大鼠（200~250 g）随机分为5组:假手术组（n=12）、SCI组（n=12）、香芹酚组（n=36）,香芹酚组根据香芹酚剂量分为低、中、高剂量3个亚组,每亚组12只。低、中、高剂量香芹酚组SCI后30 min腹腔注射香芹酚,剂量分别为10、20、40 mg/kg,每日一次;假手术组和SCI组每日腹腔注射等量生理盐水。采用Allen法建立大鼠SCI模型;假手术组只行椎板切除手术。SCI后24、48、72 h,采用BBB评分评估大鼠神经功能;SCI后72 h,采用ELISA法检测损伤脊髓组织丙二醛（MDA）、超氧化物歧化酶（SOD）、谷胱甘肽（GSH）、过氧化氢酶（CAT）、caspase-3活性;Western-blot法检测损伤脊髓组织Bax,Bcl-2蛋白表达水平。结果 SCI后,大鼠BBB评分均明显降低（P<0.05）,损伤脊髓组织水肿指数以及MDA、caspase-3和Bax水平均明显增高（P<0.05）,而SOD、GSH、CAT、Bcl-2水平均明显降低（P<0.05）;香芹酚能明显改善大鼠BBB评分（P<0.05）,明显降低水肿指数以及MDA、caspase-3和Bax水平（P<0.05）,而显著增加CAT、SOD、GSH、Bcl-2水平（P<0.05）。结论 香芹酚可通过减轻脊髓水肿、抑制氧化应激反应以及抗凋亡作用而对SCI大鼠发挥神经保护作用。     

Induction of neurofilament triplet proteins in PC12 cells by nerve growth factor

The localization of neurofilament triplet proteins in PC12 cells grown in the absence of (PC12−) or maintained in the presence of (PC12+) nerve growth factor (NGF) was studied using indirect immunofluorescence and monospecific, immunosorbent purified antibodies to 68,000 (P68), 150,000 (P150) and 200,000 (P200) dalton neurofilament proteins. The intensity of immunofluorescent staining of the triplet protein was always greater in PC12+ compared with PC12− cells. Neuritic staining was seen in PC12+ cells with all 3 monospecific antibodies to neurofilament proteins. However, the perikaryal distribution of each of the neurofilament proteins differed in both PC12+ and PC12− ells. Monospecific antibodies to P68 protein yielded a ‘ball-like’ cytoplasmic staining pattern whereas monospecific antibodies to P150 protein stained in a stippled pattern. Monospecific antibodies to P200 on the other hand diffusely stained the perikaryal cytoplasm with very faint but detectable foci of f ‘ball-like’ configurations and stippling. Electron microscopic study of PC12+ and PC12− cells revealed intermediate filaments in the cell bodies of both as well as in the processes of the former. ‘Ball-like’ clusters of such filaments were rarely seen. However, these filaments lacked the three-dimensional organization typical of intact neurofilaments.It is concluded that PC12 cells contain dissociated or incompletely assembled immunoreactive neurofilament triplet proteins and that these proteins can be induced by NGF. The PC12 cells are therefore an attractive model system not only for studies of neuronal differentiation but also for studies of neurofilament metabolism and disorders thereof.     

雷帕霉素对PC12细胞氧糖剥夺损伤的保护作用

目的探讨雷帕霉素对PC12细胞氧糖剥夺损伤(oxygen and glucose deprivation,OGD)的作用。方法选取处于对数生长期的PC12细胞,分为正常组、OGD组、溶剂组和1 nmol、10 nmol、100 nmol、500 nmol雷帕霉素组,OGD同时给予雷帕霉素处理,8 h后通过倒置显微镜观察细胞形态学的变化、MTT法检测细胞存活率的变化以及LDH活性检测细胞受损程度。结果与正常组相比,单纯OGD组细胞活性明显下降,且具有统计学意义(P0.05);与溶剂组相比,1、10、100、500 nmol雷帕霉素组细胞存活率均存在不同程度的增高,其中10、100、500 nmol组具有统计学意义(P0.05)。结论雷帕霉素对PC12细胞OGD损伤具有保护作用。     

Protective effects of sesamin and sesamolin on hypoxic neuronal and PC12 cells

Reactive oxygen species (ROS) are important mediators of a variety of pathological processes, including inflammation and ischemic injury. The neuroprotective effects of sesame antioxidants, sesamin and sesamolin, against hypoxia or H2O2-induced cell injury were evaluated by cell viability or lactate dehydrogenase (LDH) activity. Sesamin and sesamolin reduced LDH release of PC12 cells under hypoxia or H2O2-stress in a dose-dependent manner. Dichlorofluorescein (DCF)-sensitive ROS production was induced in PC12 cells by hypoxia or H2O2-stress but was diminished in the presence of sesamin and sesamolin. We evaluated further the role of mitogen-activated protein kinases (MAPKs) and caspase-3 in hypoxia-induced PC12 cell death. Extracellular signal-regulated protein kinase (ERK) 1, c-jun N-terminal kinase (JNK), and p38 MAPKs of signaling pathways were activated during hypoxia. We found that the inhibition of MAPKs and caspase-3 by sesamin and sesamolin correlated well with the reduction in LDH release under hypoxia. Furthermore, the hypoxia-induced apoptotic-like cell death in cultured cortical cells as detected by a fluorescent DNA binding dye was reduced significantly by sesamin and sesamolin. Taken together, these results suggest that the protective effect of sesamin and sesamolin on hypoxic neuronal and PC12 cells might be related to suppression of ROS generation and MAPK activation.     

Dexamethasone blocks nerve growth factor induction of nerve growth factor receptor mRNA in PC12 cells.

Glucocorticoids and nerve growth factor (NGF) have been shown to have antagonistic effects on chromaffin cells in vivo. Here we determined the effect of the synthetic glucocorticoid, dexamethasone, on levels of mRNA for the nerve growth factor receptor (NGFR) in rat PC12 pheochromocytoma cells. Following administration of dexamethasone (1 microM) there is a decline in NGFR mRNA expression. More importantly, administration of dexamethasone appears to block the NGF-mediated induction of NGFR when both agents are administered simultaneously. These data support the hypothesis that glucocorticoids and NGF act in opposition in determination of the phenotype of chromaffin cells.     

Serum vulnerability and time-dependent stabilization of neurites induced by nerve growth factor in PC12 pheochromocytoma cells

Cultures of PC12 pheochromocytoma cells were established on a polyornithine substratum in medium supplemented with the chemically defined N1 mixture in the presence or absence of Nerve Growth Factor (NGF). Normal cell proliferation in the absence of NGF was equally competent when fetal calf serum (FCS) was replaced with N1-supplemented medium. The differentiation of PC12 cells, which occurs upon NGF treatment, ultimately results in cell death without the addition of 0.1% FCS to the N1-supplemented medium. The combination of N1, 0.1% FCS, and NGF permits the PC12 cells to develop a neuritic outgrowth much earlier than when higher (1-10%) FCS levels are used. Neurite retraction is caused in a dose-dependent manner by a delayed presentation of FCS. Within 2 days of serum presentation, however, neurites regrow to achieve that percentage of neurite-bearing cells which is seen without a serum challenge. Moreover, the retraction response becomes less pronounced with time over the 8-day culture period for any given serum concentration. Among the N1 ingredients, only insulin and transferrin are needed by PC12 cells for survival whether in the dividing state or not. Neurite growth was not dependent on any of the N1 components.     

hBcl-2基因修饰的骨髓基质细胞对体外培养PC12细胞的保护作用

目的观察hBcl-2转染的骨髓基质细胞(MSCs)对体外培养PC12细胞的保护作用,为下一步hBcl-2修饰的MSCs脑内移植治疗奠定基础。方法采用密度梯度离心结合贴壁法分离、培养大鼠MSCs,对培养第3代的MSCs进行鉴定;hBcl-2用脂质体转染MSCs建立MSCs-hBcl-2基因工程细胞;用H2O2建立PC12细胞氧化应激损伤模型;MTT法检测MSCs-hBcl-2基因工程细胞上清对体外培养的PC12细胞活性的影响。结果成功培养出MSCs细胞,免疫组化结果显示培养的细胞CD44、CD71表达阳性,而CD45表达阴性;建立了有稳定高效hBcl-2表达的MSCs-hBcl-2基因工程细胞,并观察到MSCs-hBcl-2基因工程细胞较MSCs更能减轻PC12细胞的氧化损伤(P<0.05)。结论hBcl-2基因修饰的MSCs对PC12细胞的生长、生存有着重要的保护作用。     

活化小胶质细胞对PC12细胞中CREB激活程度影响的研究

目的探讨小胶质细胞活化后是否影响神经细胞（PC12细胞）中cAMP反应蛋白元件结合蛋白（CREB）的活化程度。方法原代细胞培养法培养小胶质细胞。传代培养PC12细胞．IFN-1激活小胶质细胞后利用转移筛网使其与PC12细胞共育，经不同时间段（15min、2h、24h）共育后Westernblot检测PC12细胞的总CREB和磷酸化CREB，考察CREB活化程度。结果激活小胶质细胞与PC12细胞共育后15min。即有CREB活化程度的显著增高．同PC12细胞组相比差异显著（P〈0．05），此后随时间延长其活化程度逐渐下降，2h时已无统计学差异，24h时甚至略低于PC12细胞组。结论激活小胶质细胞能够在短时间内迅速一过性提高神经细胞中活化CREB含量，为增强神经细胞抗损伤能力奠定基础。     

Role of low-affinity p75 receptor in nerve growth factor-inducible growth arrest of PC12 cells

Mutant PC12 cell clones (PC84 cells) were obtained by transfection with nerve growth factor (NGF) cDNA. These cells secreted active NGF, extended short processes, and proliferated faster than the parental PC12 cells. These features are of great interest because the parental PC12 cells cease proliferation and extend long processes when transfected with NGF cDNA. PC84 cells expressed a high level of acetylcholinesterase activity and neurofilament M, which indicates that PC84 cells were differentiated. The inhibition of TrkA by K252a diminished the short processes of PC84 cells but had no effect on their fast proliferation. The expression level of TrkA in PC84 cells was comparable to that in PC12 cells; whereas that of another NGF receptor, p75, was significantly lower. These data suggest that the decrease of p75 contributed to the continuous growth of PC84 cells, which was confirmed by suppressing p75 activity of PC12 cells with the antisense oligonucleotide of p75 or with anti-p75 neutralizing antibody. The treated cells did not cease proliferation in the presence of NGF and extended short processes. Our results suggest that NGF signaling via TrkA affects the differentiation characteristics of PC12 cells but that an additional signaling via p75 is necessary for the growth arrest of the cells.     

神经干细胞移植治疗缺氧缺血性脑损伤的实验研究

目的 研究神经干细胞移植治疗缺氧缺血性脑损伤的可行性。方法 取孕龄为12－16天的母鼠，从胎脑中分离神经细胞，进行培养、鉴定。用出生7天的SD大鼠的新生鼠制作缺氧缺血性脑损伤的动物模型，7天后接受神经干细胞移植（移植组，n＝16只），同时设置对照组，只注射磷酸缓冲液（对照组，n=8只），8－10周后，作Y迷宫实验检测大鼠的学习能力和记忆能力。取脑组织作免疫组织化学检查。结果 从大鼠胎脑中成功培养出神经干细胞，培养条件下呈悬浮状态生长，形成神经球，绝大多数的细胞表达神经干细胞的标志物神经巢蛋白（nestin）。接爱神经干细胞移植组大鼠的学习能力、记忆能力和对照组相比，有明显提高，差异具有显著性（P＜0.05）。接受神经干细胞移植大鼠组织中可见存活的移植细胞，并和宿主脑组织融合在一起。结论 在体外培养条件下，可从胎脑组织中培养出神经干细胞，移植到缺氧缺血性脑损伤大鼠脑内后，细胞与宿主的脑组织融合在一起，动物的学习、记忆能力有改善。移植神经干细胞是治疗缺氧缺知性脑损伤的有效方法之一。     

Decreased levels of nerve growth factor receptor on dexamethasone-treated PC12 cells

Treatment of PC12 cells with dexamethasone leads, in a period of days, to a 60% decrease in the binding of (125I)nerve growth factor. The decrease was maximal after 3 days of treatment with 1 microM dexamethasone, but some decrease was seen after 6 hr and at concentrations as low as 10 nM. The effect was specific for the glucocorticosteroids. Scatchard plots confirmed the overall loss of nerve growth factor binding, and studies with trypsin digestion and Triton X-100 extraction indicated that the decrease in binding was largely due to a decrease in the number of low-affinity receptors. Nerve growth factor-induced changes, such as the induction of ornithine decarboxylase and the generation of neurites, were inhibited, but only minimally, in dexamethasone-treated cells.