Lateral ventricular liponeurocytoma: Review of literature and case illustration

BackgroundLiponeurocytoma is an uncommon tumor of the central nervous system. It is very rare for this tumor to originate within the lateral ventricle. In the context of the rarity of this tumor entity, this review article aims to summarize the clinical, radiological, and pathological features of lateral ventricular liponeurocytoma to facilitate its diagnosis and management.MethodsHere, we conduct a systematic literature review using the Pubmed, Scopus, and Cochrane Library database for all cases of lateral ventricular liponeurocytoma. A case illustration complements this review.ResultsThe described cases from 1997 onward include 14 cases that have been published in full papers in the English literature. Six additional cases are reported in short English abstracts in full non-English papers, and one case was described in a central neurocytoma report. There is a definite male predominance of 70% (14 male) and a mean age of 37 years (range 24–62). Heterogenous enhancement and signals in magnetic resonant images (MRI) are the radiological characteristics. In all reported cases, the presence of lipocytes and fat vacuoles is considered the paramount histopathological feature. Total surgical resection was achieved in 80% (12 out of 15) of the cases. Only two cases (including ours) received radiation therapy. Recurrence was seen in two patients during follow-up that was treated by radiation therapy in one and surgery in the other. The proliferation index is mostly below 5% in all cases, with the Ki-67 range between < 1% to 10%.ConclusionsLateral ventricular liponeurocytoma has been treated effectively by surgical resection in a limited number of cases. The decision for radiation therapy is based on a high proliferation index and tumor recurrence.     

雪旺细胞外泌体影响胶质瘢痕形成修复小鼠脊髓损伤的实验研究

目的:探讨雪旺细胞外泌体（SCDEs）对小鼠脊髓损伤的修复作用。方法:从小鼠坐骨神经中提取原代雪旺细胞,并将雪旺细胞培养上清分次超速离心得到雪旺细胞外泌体。透射电镜鉴定外泌体 ,尾静脉注射外泌体,每周2次,每次3 μL/只,BMS评分观察小鼠行为学功能恢复,免疫荧光染色观察外泌体神经保护作用和胶质瘢痕变化情况。结果:SCDEs的直径范围为40~100 nm;与PBS组相比, SCDEs组行为学BMS评分增加（P<0.05）,神经学功能指标有所恢复（P<0.01）,胶质瘢痕增加（P<0.01）。结论:SCDEs可以促进损伤后胶质瘢痕的增加,修复脊髓损伤。     

嗅鞘细胞移植联合应用GDNF对大鼠视神经不全损伤后功能恢复的作用

目的:探讨嗅鞘细胞(OEC)移植和人重组胶质细胞源性神经营养因子(recombinant human glial cell line-derived neurotrophic factor,rhGDNF)对大鼠视神经不全损伤后功能恢复的作用.方法:采用无创血管夹在成年大鼠制作视神经不全损伤模型,分为玻璃体腔注射rhGDNF、视神经损伤处注射OEC、rhGDNF OEC联合治疗组和对照组.在损伤前、损伤后即刻及伤后1,2,4,8和12wk检测伤眼闪光视觉诱发电位.结果:视神经损伤后即刻闪光视觉诱发电位波形呈熄灭状.伤后1wk各治疗组和对照组潜伏期基本恢复至损伤前水平.振幅恢复缓慢,伤后1～2 wk治疗组与对照组比较无显著差异(P＞0.05);4wk以后rhGDNF组和OEC组与对照相比间差异显著(P＜0.05),GDNF OEC组与对照组相比差异非常显著(P＜0.01).8wk时对照组恢复至损伤前的43.1%,GDNF治疗组恢复至损伤前的51.5%,OEC治疗组恢复至损伤前的57.4%,而GDNF OEC联合治疗组恢复至损伤前的68.7%,12wk后达75%.结论:嗅鞘细胞(OEC)移植和rhGDNF对大鼠视神经不全损伤后视神经功能的恢复有明显的促进作用,二者联合治疗效果更显著.     

复方地黄对帕金森病大鼠多巴胺能神经元及GDNF表达的影响

目的:研究复方地黄对6-羟基多巴胺(6-hydroxydopamine,6-OHDA)诱导的帕金森病(Parkinson’s disease,PD)大鼠多巴胺能神经元的保护作用及其可能机制。方法:40只SD雄性大鼠,分为正常组、假手术组、模型组、模型组+复方地黄组(即干预组)。观察PD大鼠药物诱发的旋转行为;免疫组化法观察黑质酪氨酸羟化酶(tyrosine hydroxylase,TH)阳性神经元数目及胶质细胞源性神经营养因子(glial cell line-derivedneurotrophic factor,GDNF)表达水平的变化。结果:干预组与模型组间的旋转圈数有明显差异(P0.05);模型组黑质TH阳性神经元数目(52.9±2.2)明显少于正常组(160.3±2.4)、假手术组(161.6±3.4)及干预组(61.5±2.6)(P0.05);在大鼠黑质和纹状体部位,干预组GDNF阳性细胞数量比正常组、假手术组、模型组均明显增加(P0.05)。结论:复方地黄方能明显改善PD大鼠的旋转行为,拮抗6-羟基多巴胺诱导的PD大鼠黑质多巴胺能神经元的丢失,其保护作用可能与促进内源性GDNF分泌增加有关。     

Reactive astroglia-neuron relationships in the human cerebellar cortex: A quantitative, morphological and immunocytochemical study in Creutzfeldt-Jakob disease

In order to investigate the role of neuron-glia interactions in the response of astroglial to a non-invasive cerebellar cortex injury, we have used two cases of the ataxic form of Creutzfeldt-Jakob disease (CJD) with distinct neuronal loss and diffuse astrogliosis. The quantitative study showed no changes in cell density of either Purkinje or Bergmann glial cells in CJ-1, whereas in the more affected CJ-2 a loss of Purkinje cells and an increase of Bergmann glial cells was found. The granular layer in both CJD cases showed a similar loss of granule cells (about 60% ) in parallel with the significant increase in GFAP+ reactive astrocytes. GFAP immunostaining revealed greater reactivity of Bergmann glia in CJ-2 than in CJ-1, as indicated by the thicker glial processes and the higher optical density. Granular layer reactive astrocytes were regularly spaced. In both CJD cases there was strict preservation of the spatial arrangement of all astroglial subtypes—Fañanas cells, Bergmann glia and granular layer astrocytes. Reactive Fañanas and Bergmann glial cells and microglia/macrophages expressed vimentin, while only a few vimentin+ reactive astrocytes were detected in the granular layer. Karyometric analysis showed that the increase in nuclear volume in reactive astrloglia was directly related with the level of glial hypertrophy. The number of nucleoli per nuclear section was constant in astroglial cells of human controls and CJD, suggesting an absence of polyploidy in reactive astroglia. Ultrastructural analysis revealed junctional complexes formed by the association of macula adherens and gap junctions. In the molecular layer numerous vacant dendritic spines were ensheathed by lamellar processes of reactive Bergmann glia. Our results suggest that quantitative (neuron/astroglia ratio) and qualitative changes in the interaction of neurons with their region-specific astroglial partners play a central role in the astroglial response pattern to the pathogenic agent of CJD.     

急性高眼压大鼠视网膜胶质细胞水通道蛋白-4的内化

目的:观察急性高眼压时大鼠视网膜胶质细胞水通道蛋白-4(AQP4)内化的时空变化及其规律,并探讨其与视网膜水肿的关系.方法:建模并分组;应用免疫荧光双标鉴定视网膜AQP4阳性细胞;观察AQP4与早期内涵体抗原1(EEA1)及晚期内涵体标记物甘露糖-6-磷酸受体(MPR)的共表达规律.结果:在正常视网膜内,表达AQP4的星形胶质细胞胞体位于节细胞层,Müller细胞的胞体位于内核层.正常及假手术组未见AQP4与EEA-1、MPR的共表达;高眼压作用不同时间,AQP4与EEA1共表达细胞的分布部位及其占AQP4阳性细胞比例都有改变,在高眼压作用60 min,AQP4与EEA1共表达细胞的比例达到最高值,AQP4与MPR共表达细胞分布的部位也有变化.结论:高眼压可诱导视网膜胶质细胞AQP4的内化,即AQP4经过内吞进入早期内涵体,再转运至晚期内涵体.AQP4的内化可能对肿胀的胶质细胞起保护作用.     

Lactulose enhances neuroplasticity to improve cognitive function in early hepatic encephalopathy

Lactulose is known to improve cognitive function in patients with early hepatic encephalopathy; however, the underlying mechanism remains poorly understood. In the present study, we investigated the behavioral and neurochemical effects of lactulose in a rat model of early hepatic encephalopathy induced by carbon tetrachloride. Immunohistochemistry showed that lactulose treatment promoted neurogenesis and increased the number of neurons and astrocytes in the hippocampus. Moreover, lactulose-treated rats showed shorter escape latencies than model rats in the Morris water maze, indicating that lactulose improved the cognitive impairments caused by hepatic encephalopathy. The present findings suggest that lactulose effectively improves cognitive function by enhancing neuroplasticity in a rat model of early hepatic encephalopathy.     

Purinergic transmission and transglial signaling between neuron somata in the dorsal root ganglion

Most dorsal root ganglion neuronal somata (NS) are isolated from their neighbours by a satellite glial cell (SGC) sheath. However, some NS are associated in pairs, separated solely by the membrane septum of a common SGC to form a neuron–glial cell–neuron (NGlN) trimer. We reported that stimulation of one NS evokes a delayed, noisy and long‐duration inward current in both itself and its passive partner that was blocked by suramin, a general purinergic antagonist. Here we test the hypothesis that NGlN transmission involves purinergic activation of the SGC. Stimulation of the NS triggered a sustained current noise in the SGC. Block of transmission through the NGlN by reactive blue 2 or thapsigargin, a Ca²⁺ store‐depletion agent, implicated a Ca²⁺ store discharge‐linked P2Y receptor. P2Y2 was identified by simulation of the NGlN‐like transmission by puffing UTP onto the SGC and by immunocytochemical localization to the SGC membrane septum. Block of the UTP effect by BAPTA, an intracellular Ca²⁺ scavenger, supported the involvement of SGC Ca²⁺ stores in the signaling pathway. We infer that transmission through the NGlN trimer involves secretion of ATP from the NS and triggering of SGC Ca²⁺ store discharge via P2Y2 receptors. Presumably, cytoplasmic Ca²⁺ elevation leads to the release of an as‐yet unidentified second transmitter from the glial cell to complete transmission. Thus, the two NS of the NGlN trimer communicate via a ‘sandwich synapse’ transglial pathway, a novel signaling mechanism that may contribute to information transfer in other regions of the nervous system.