Ethanol impairs Rho GTPase signaling and differentiation of cerebellar granule neurons in a rodent model of fetal alcohol syndrome

Developmental exposure to ethanol impairs fetal brain development and causes fetal alcohol syndrome. Although the cerebellum is one of the most alcohol-sensitive brain areas, signaling mechanisms underlying the deleterious effects of ethanol on developing cerebellar granule neurons (CGNs) are largely unknown. Here we describe the effects of in vivo ethanol exposure on neurite formation in CGNs and on the activation of Rho GTPases (RhoA and Rac1), regulators of neurite formation. Exposure of 7-day-old rat pups to ethanol for 3 h moderately increased blood alcohol concentration (BAC) (∼40 mM) and inhibited neurite formation and Rac1 activation in CGNs. Longer exposure to ethanol for 5 h resulted in higher BAC (∼80 mM), induced apoptosis, inhibited Rac1, and activated RhoA. Studies demonstrated a regulatory role of Rho GTPases in differentiation of cerebellar neurons, and indicated that ethanol-associated impairment of Rho GTPase signaling might contribute to brain defects observed in fetal alcohol syndrome. Received 16 July 2006; received after revision 12 September 2006; accepted 13 October 2006     

发热信号传导途径及诊断程序研究

目的研究发热防治新原则和感染性发热诊断新程序。方法运用医学统计学原理,对开放性学术信息综合分析。结果多种致热性细胞因子和负调节介质共同作用,使机体温核集团对致热原作用发生指向性调控。讨论外源性致热原通过神经介质、致热性细胞因子及内源性致热原作用体温中枢,最终导致体温升高。     

新纹状体棘神经元的自发放模式

在细胞水平上，对纹状体棘细胞自发放模式的产生机制进行了综述，并在此基础上作了若干合理推断．     

Effect of Thrombin on the Apoptosis of Hippocampal Neurons in vitro

Hippocampal neurons were treated by thrombin and thrombin receptor activating peptides (TRAP). Cell survival rate was decreased in a dose-dependent manner by MTT assay. The numbers of apoptotic cell and apoptotic rate of hippocampal neurons treated by different concentrations of thrombin were increased in a dose-dependent manner by terminal deoxynucleotidyl transferase (TdT) mediated dUTP-biotin nick end-labeling (TUNEL) method and Flow Cytometry. When the concentration of thrombin is 40 U/mL, TUNEL positive cells and apoptotic rate of hippocampal neurons reached peak value, were 27. 3 4.0 and (29.333 4.633 ) %, respectively. Immunocytochemistry assay show that Bcl-2 protein expression was down- regulated and Bax protein expression was up-regulated with the concentration of thrombin increased. TRAP can mimic the effect of thrombin to induce apoptosis on hippocampal neurons. These data demonstrated that thrombin induced hippocampal neuron apoptosis in a dose-dependent manner through activating protease-activated protein-1 (PAR-1). The change in expression of Bcl-2 and Bax was related with the effect of high concentration thrombin induced apoptosis on hippocampal neurons.     

成年小白鼠新生神经元的观察

将 3[H]标记的胸腺嘧啶核苷 (3[H]-thymidine)注入成年小白鼠腹腔 ,大脑中的神经细胞有丝分裂 ,可通过放射自显影在新生神经细胞中以银粒方式显现 3[H]标记 ,在光镜下观察脑切片中的银粒细胞即为新生神经元 .本实验利用放射自显影的方法 ,在成年小白鼠的海马和嗅球区域观察到新生神经元 .     

触角嗅觉神经束路示踪的赖氨酸钴填充方法

应用赖氨酸钴填充技术 ,观察雄蛾触角嗅觉神经的传入途径及向中枢投射踪迹的方法和操作程序。结果显示赖氨酸钴填充的神经元成黑色 ,与周围环境反差较大 ,清晰易辨 ,能准确反映触角神经元的生理特性及其向中枢投射位置     

蟋蟀下行脑神经元形态与功能的研究进展

蟋蟀下行脑神经元通过围咽神经索将编译、整合的信息传递到腹、胸等神经节的运动中枢,约占脑神经元总量的0.3‰~1.5‰,并能高效的聚集信息.传递触角感觉信息的下行脑神经元分支多聚集在中脑;外界刺激信息通过下行脑神经元传递到运动中枢支配行走,同时不断接收听觉、视觉信息调整行走的速度和方向.研究下行脑神经元的形态结构与功能将为研究昆虫微小脑的控制原理提供重要的理论依据.     

Long-term depressor effects of noradrenaline and dopamine neurons transplanted into the third ventricle of the brain of salt-loaded hypertensive rats

Summary Neural tissues including A 6 group noradrenaline neurons in the locus ceruleus or A 10 group dopamine neurons in the substantia nigra were transplanted into the third ventricle at the preoptic-anterior hypothalamic level of rats made hypertensive by salt loading. Either transplant exerted a long-lasting depressor effect.     

野木瓜注射液对小鼠皮层神经细胞的抗氧化保护作用

研究了野木瓜注射液(IS)对小鼠大脑皮层神经细胞氧化损伤的保护作用.在细胞培养液中加入100μmol/L H2O2和不同浓度IS,培养数日后通过观察细胞的形态变化,检测细胞外液LDH的活力,胞内超氧化物歧化酶(SOD)的活性,测定细胞活性来观测IS对氧化受损神经细胞的保护作用,并通过脱氧核糖法对IS的羟自由基(.OH)清除率进行测定.结果表明:浓度在25～300 mg/L,IS均能抑制神经细胞的氧化损伤,神经细胞SOD酶活力上升,细胞外液LDH活力降低,浓度为100 mg/L时效果最显著.与阳性对照甘露醇相比,IS有较高的.OH清除率.IS有较高的抗氧化能力,能有效抑制H2O2导致的皮层神经细胞的损伤.     

野木瓜注射液及其提取物对脊髓神经元的氧化保护和生长促进

研究野木瓜注射液(IS)及其提取物(AI)对氧化损伤脊髓神经元的保护和对未损伤脊髓神经元生长的影响.方法:通过MTT法和细胞外液LDH漏出量的测定检测IS对未损伤的脊髓神经元细胞存活率的影响;建立H2O2氧化损伤模型,通过MTT法、胞内SOD活力和细胞外液LDH漏出量的测定研究IS对H2O2氧化损伤脊髓神经元的细胞保护作用;运用激光共聚焦显微镜研究氧化受损及IS保护对脊髓神经元胞浆内Ca2+浓度变化的影响.结果表明:当浓度为100～200 mg/L时,IS能显著地促进离体培养的小鼠脊髓神经元氧化受损的修复,神经元存活率得到显著的提高,胞内SOD活力显著地增加和LDH漏出量显著地减少,同时胞内Ca2+超载显著地被抑制;未受损的脊髓神经元在200 mg/L IS作用下LDH漏出量显著地减少,细胞存活率显著地提高;AI3对能显著地提高氧化受损脊髓神经元的存活率.