晚发性抑郁患者情绪调节机制的ERPs研究

目的采用事件相关电位探讨晚发性抑郁患者情绪调节障碍的神经生理机制。方法被试者包括16例晚发性抑郁患者（发病年龄≥60岁）与16名健康老年人。采用Go／Nogo实验范式，要求被试者对刺激序列中双个三角形进行按键反应（Go），单个三角形不反应（Nogo）。记录32导脑电。结果健康老年人中，Nogo刺激产生了明显的额中央区分布的N2Nogo和P3Nogo；与对照组相比，病例组的N2Nogo。波幅明显增高，而P3Nogo波幅显著降低，两者潜伏期无显著差异。结论晚发抑郁患者存在情绪调节障碍，其电生理学指标为N2Nogo明显增高和P3Nogo的显著降低，为晚发性抑郁的诊断和治疗提供了一定的客观评价指标。     

Effects of ISI and stimulus probability on event-related go/nogo potentials after somatosensory stimulation

The present study investigated the characteristics of the middle-latency negative potential of event-related potentials (ERPs) using somatosensory go/nogo tasks. We manipulated interstimulus interval (ISI) in Experiment 1 and stimulus probability in Experiment 2 and analyzed the subtracted difference waveform resulting from subtraction of the ERP evoked by the go stimulation from that evoked by the nogo stimulation. In Experiment 1, the peak latency of negativity became significantly longer as the ISI increased, but the peak amplitude was unchanged. The reaction time (RT) was longer with increasing ISI. In Experiment 2, manipulation of the stimulus probability yielded an increase in peak amplitude with decreasing probability of the nogo stimulus, but did not affect the latency. The RT increased as the probability of a nogo stimulus rose. Because manipulation of the ISI and stimulus probability elicited different brain activities, we hypothesized that manipulation of the ISI elicited a delay of the stimulus evaluation process including response inhibition, and that stimulus probability significantly affected the strength of the response inhibition process.     

Nogo(N-18)在大鼠脑干及小脑分布的免疫组织化学研究

采用免疫组织化学方法(SP法),研究了Nogo(N-18)在大鼠脑干及小脑的分布并探讨其存在的意义。结果表明,Nogo(N-18)在正常大鼠脑干以及小脑的神经核团有广泛的表达,阳性物质很强地表达于神经元的胞核内,神经元胞体、突起内表达较弱。结论:Nogo(N-18)在脑干及小脑的神经核团广泛表达提示其作为一种髓鞘源性神经突生长抑制因子在中枢神经系统中的存在,可能在正常的神经活动中起重要作用。     

Nogo‐B expression,in arterial intima,is impeded in the early stages of atherosclerosis in humans

Nogo‐B (Reticulon 4B) is considered to be a novel vascular marker, which may have a protective role in injury‐induced neointima formation and atherosclerosis. Nogo A/B is found to be crucial for monocyte/macrophage recruitment in acute inflammation and it is expressed in CD68 + macrophages. We hypothesize that macrophage infiltration in atherosclerosis is not dependent on Nogo‐B expression in arterial wall. We have assessed Nogo‐B expression and macrophage accumulation in the iliac arteries of healthy organ donors and organ donors with cardiovascular risk factors. Paraffin sections of 66 iliac arteries, from 44 deceased organ donors (17 women and 27 men), were studied. The healthy and cardiovascular risk (CVR) subgroups were created. With regard to staging of the atherosclerotic process, the thickness of arterial intima was measured in digitalized images of H+E stained tissue sections. Immunohistochemical reactions (Nogo‐B and CD68) were carried out in all arteries (66 samples). Western blotting (WB‐19 samples) and real‐time PCR (27 samples) were performed on selected arteries. Significantly higher Nogo‐B expression was demonstrated in the intima of the healthy subjects' subgroup, using immunohistochemistry. WB and real‐time PCR revealed a trend toward lower Nogo‐B expression in the adventitia of the CVR subgroup. Furthermore, the thickness of the intima was found to negatively correlate with the expression of Nogo‐B in the intima and media (r = ?0.32; p < 0.05; r = ?0.32; p < 0.05). Macrophage infiltrates were more prominent in intima of CVR subjects (0.65 vs 3.52 a.u.; p < 0.01). Macrophage density in intima increased with atherosclerosis progression (r = 0.37; p < 0.01). CD68 macrophages density in adventitia was lower in CVR arteries than in healthy arteries. The expression of Nogo‐B, in arterial intima, is impeded in the early stages of atherosclerosis. Accumulation of arterial intimal CD68 macrophages has been shown to progress; however, the overall macrophage density in the adventitia is reduced in arteries shown to have intimal thickening. Macrophage infiltration is not accompanied by Nogo‐B expression in atherosclerotic arteries.     

Expression pattern of Nogo‐A,MAG, and NgR in regenerating urodele spinal cord

Background: The mammalian central nervous system is incapable of substantial axon regeneration after injury partially due to the presence of myelin‐associated inhibitory molecules including Nogo‐A and myelin associated glycoprotein (MAG). In contrast, axolotl salamanders are capable of considerable axon regrowth during spinal cord regeneration. Results: Here, we show that Nogo‐A and MAG, and their receptor, Nogo receptor (NgR), are present in the axolotl genome and are broadly expressed in the central nervous system (CNS) during development, adulthood, and importantly, during regeneration. Furthermore, we show that Nogo‐A and NgR are co‐expressed in Sox2 positive neural progenitor cells. Conclusions: These expression patterns suggest myelin‐associated proteins are permissive for neural development and regeneration in axolotls. Developmental Dynamics 242:847–860, 2013. © 2013 Wiley Periodicals, Inc.     

Neuronal Nogo‐A in New‐born Retinal Ganglion Cells: Implication for the Formation of the Age‐related Fiber Order in the Optic Tract

Nogo‐A is highly expressed in oligodendrocytes in the adult central nervous system (CNS). Recently it was found that Nogo‐A is also expressed in some neuronal types during development. Here, we examined the expression pattern of Nogo‐A in both the retina and optic tract (OT) of mouse embryos from E12 to E15. After perturbation of its function in the OT for 5 hr in the brain slice culture system using a Nogo‐A specific antibody or antagonist of its receptor (NEP1‐40), the optic nerve fibers and growth cones were traced with DiI. We showed that most Tuj‐1 positive new‐born neurons at E12 were Nogo‐A positive. At E15, retinal neurons reduced the Nogo‐A expression. It was worth noting that some projecting axons expressed Nogo‐A along the retinofugal pathway. On the basis of their specific locations within the superficial half of the OT and the colocalization with GAP‐43 (a marker for the newly born growth cones and axons), we concluded that those Nogo‐A positive axons were the newly arrived retinal fibers. Blocking the function of Nogo‐A with Nogo‐A antibody or NEP1‐40 resulted in the shift of DiI labeled axons and growth cones from the superficial half to the whole depth of the OT. These results indicate that Nogo‐A in the newly born retinal ganglion cells (RGCs) and their axons are involved in sorting out the newly arrived axons to the subpial region of the OT. Anat Rec, 299:1027–1036, 2016. © 2016 Wiley Periodicals, Inc.     

电针对脊髓损伤大鼠 Nogo/NgR 信号通路相关因子基因表达的影响

目的观察电针对脊髓损伤大鼠Nogo/NgR信号通路相关因子基因表达变化,探讨电针治疗脊髓损伤的可能作用机制。方法大鼠随机分为模型组、电针组、阻断剂组、电针+阻断剂组、假手术组,用改良Allen’s撞击法制备T10脊髓损伤模型,分别于治疗后1、7、14 d对各组大鼠进行BBB功能评分;在7、14 d于损伤处提取脊髓组织,以蛋白印迹法(Western blot)测定各组大鼠脊髓组织中Nogo-A、NgR、LINGO-1蛋白的表达变化,实时荧光定量PCR测定Nogo-A、NgR、LINGO-1 mRNA的表达变化。结果脊髓损伤后,造模大鼠1 d后BBB评分均为0分;治疗7、14 d后,各治疗组BBB评分均明显高于模型组(P0.05),且电针+阻断剂组优于电针组、阻断剂组(P0.05)。与假手术组比较,同时间点模型组各基因表达均明显提高(P0.05);与模型组比较,各治疗组基因表达明显下降(P0.05);电针+阻断剂阻组与电针组比较,同时间点LINGO-1基因表达有显著差异(P0.05)。结论 Nogo/NgR信号通路在脊髓损伤后神经的再生与修复过程中起着关键作用,电针通过抑制Nogo/NgR信号通路而对脊髓损伤大鼠起治疗作用。     

Relations between catechol-O-methyltransferase Val158Met genotype and inhibitory control development in childhood

The Val158Met rs4680 single-nucleotide polymorphism (SNP) at the catechol-O-methyltransferase (COMT) gene, primarily involved in dopamine breakdown within prefrontal cortex, has shown relations with inhibitory control (IC) in both adults and children. However, little is known about how COMT genotype relates to developmental trajectories of IC throughout childhood. Here, our study explored the effects of the COMT genotype (Val/Val, Val/Met, and Met/Met) on IC trajectories between the ages of 5 and 10 years. Children (n = 222) completed a Go/Nogo task at ages 5, 7, and 10; IC was characterized using signal detection theory to examine IC performance (d′) and response strategy (RS) (criterion). COMT genotype was not related to initial levels of IC performance and RS at age 5 or change in RS from ages 5 to 10. In contrast, COMT genotype was related to change in IC performance between 5 and 10 years. While Val/Val children did not differ from Val/Met children in development of IC performance, children with the Met/Met genotype exhibited more rapid development of IC performance when compared with Val/Met peers. These results suggest that COMT genotype modulates the development of IC performance in middle childhood.