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| 1 | Infection,Pain,and Itch显示文摘Pain and itch are unpleasant sensations that often accompany infections caused by viral, bacterial,parasitic, and fungal pathogens. Recent studies show that sensory neurons are able to directly detect pathogens to mediate pain and itch. Nociceptor and pruriceptor neurons respond to pathogen-associated molecular patterns,including Toll-like receptor ligands, N-formyl peptides,and bacterial toxins. Other pathogens are able to silence neuronal activity to produce analgesia during infection.Pain and itch could lead to neuronal modulation of the immune system or behavioral avoidance of future pathogen exposure. Conversely, pathogens could modulate neuronal signaling to potentiate their pathogenesis and facilitate their spread to other hosts. Defining how pathogens modulate pain and itch has critical implications for sensory neurobiology and our understanding of hostmicrobe interactions. | Isaac M.Chiu | 2018 | Neuroscience Bulletin2018，34，1： | 7 |
| 2 | PYNOD对LPS活化的BV2小胶质细胞炎症因子释放的影响显示文摘目的:观察PYNOD对LPS活化的BV2小胶质细胞炎症因子释放的影响。方法:将表达PYNOD的重组质粒p EGFP-C2-PYNOD瞬时转染BV2细胞后,加入LPS作用24 h,Griess法检测一氧化氮(nitric oxide,NO)的释放,实时荧光定量PCR(real-time PCR)检测诱导型一氧化氮合酶(inducible NO synthase,i NOS)和白细胞介素-1β(interleukin-1β,IL-1β)mRNA的表达,此外Western blotting和ELISA法检测i NOS和IL-1β的蛋白表达。结果:转染PYNOD重组质粒能显著抑制LPS诱导的BV2小胶质细胞炎症因子NO的释放(P<0.05)。Real-time PCR证实PYNOD可抑制i NOS和IL-1β的mRNA表达,差异有统计学意义(P<0.05)。ELISA和Western blotting证实PYNOD可下调i NOS和IL-1β蛋白的表达(P<0.05)。结论:PYNOD蛋白可以在转录水平和翻译水平显著抑制LPS刺激的BV2小胶质细胞活化产生的炎症反应。 | 曾琪 戚仁斌 胡巢凤 陆大祥 | 2014 | 中国病理生理杂志2014，30，11： | 4 |
| 3 | CSF Brain-Reactive Autoantibodies are Elevated in Patients with Viral Encephalitis显示文摘Dear Editor,Brain-reactive autoantibodies are thought to play an important role in mediating disorders of the central nervous system(CNS).These antibodies direct the processes underlying several diseases,such as multiple sclerosis(MS),neuromyelitis optica(NMO),and neuropsychiatric systemic lupus erythematosus[1-3].In infectious diseases of the CNS,the pathogen itself is regarded to play a major role in the pathogenesis[4]. | Zhong-Yuan Yu Jian-Hong Wang Wei-Wei Li Ye-Ran Wang Noralyn B.Manucat-Tan Jun Wang Ju Wang Gao-Yu Cui Jie-Xiang Pan Shui-Xian Zhang Zu-Juan Liu Liang Tan Yu-Hui Liu | 2020 | Neuroscience Bulletin2020，36，8： | 3 |
| 4 | Radio Electric Asymmetric Conveyer Technology Modulates Neuroinflammation in a Mouse Model of Neurodegeneration显示文摘In this study, the effects of Radio Electric Asymmetric Conveyer(REAC), a non-invasive physical treatment, on neuroinflammatory responses in a mouse model of parkinsonism induced by intoxication with1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP),were investigated in vivo. We found that the REAC tissue optimization treatment specific for neuro-regenerative purposes(REAC TO-RGN-N) attenuated the inflammatory picture evoked by MPTP-induced nigro-striatal damage inmice, decreasing the levels of pro-inflammatory molecules and increasing anti-inflammatory mediators. Besides, there was a significant reduction of both astrocyte and microglial activation in MPTP-treated mice exposed to REAC TORGN-N. These results indicated that REAC TO-RGN-N treatment modulates the pro-inflammatory responses and reduces neuronal damage in MPTP-induced parkinsonism. | Maria Antonietta Panaro Alessandra Aloisi Giuseppe Nicolardi Dario Domenico Lofrumento Francesco De Nuccio Velia La Pesa Antonia Cianciulli Rosaria Rinaldi Rosa Calvello Vania Fontani Salvatore Rinaldi | 2018 | Neuroscience Bulletin2018，34，2： | 3 |
| 5 | Toll样受体2与缺血性脑损伤显示文摘本文阐述了Toll样受体2的分子生物学特性和信号通路,以及在脑缺血后神经元和血脑屏障损伤中的作用研究进展。 | 丁晓蔚 孟强 | 2015 | 国际脑血管病杂志2015，23，12： | 2 |
| 6 | 达珀利奈抑制急性缺血性脑卒中小鼠皮层神经炎症、胶质细胞活化及SARM1表达显示文摘目的探讨达珀利奈[(E)-Daporinad,FK866]对急性缺血性脑卒中皮层神经炎症、胶质瘢痕增生的影响与机制。方法实验动物分为假手术组(Sham组)、缺血损伤手术组(Vehicle组)和缺血手术后给予FK866干预组(FK866组),每组8只。尼氏染色检测小鼠大脑皮层缺血损伤程度,TUNEL染色检测神经元凋亡,圆筒试验和网格爬行试验检测小鼠运动、协调能力,免疫组织化学染色检测小鼠大脑皮层缺血部位离子化钙结合适配体分子1(ionized calcium-binding adapter molecule 1,Iba1)与胶质纤维酸性蛋白(glial fibrillary acidic protein,GFAP)的表达,免疫印迹检测小鼠大脑皮层Iba1、诱导型一氧化氮合酶(inducible nitric oxide synthase,iNOS)、分化簇206(cluster of differentiation 206,CD206)、GFAP、胶质瘢痕标记物磷酸蛋白聚糖(phosphacan)α和Toll/白细胞介素受体结构域的蛋白1(sterile alpha and TIR motif-containing protein 1,SARM1)的表达。结果与Vehicle组相比,FK866组小鼠大脑皮层缺血灶面积减少,凋亡神经元细胞数量减少,小鼠的运动、协调功能增强,缺血灶部位小胶质细胞及星形胶质细胞的活化减弱,Iba1、iNOS、GFAP和phosphacan蛋白表达水平降低,CD206蛋白水平增高,SARM1的蛋白水平下降。结论在缺血性脑卒中急性期,FK866减轻病灶处的神经元损伤并发挥神经保护作用,可能是通过降低SARM1的表达进而促进小胶质细胞向M2型极化并抑制胶质瘢痕的形成。 | 崔迈尹 付艳琼 李卓丽 陈吴越 廖敏 陈佰慧 | 2022 | 中国组织化学与细胞化学杂志2022，31，2： | 1 |
| 7 | Toll样受体及其在脑皮质发育不良形成中的研究进展显示文摘脑皮质发育不良(CD)是由胚胎早期神经前体细胞增殖、分化、迁移及突触、神经网络形成异常引起,目前免疫炎症机制被认为与CD的形成密切相关。而Toll样受体(TLRs)是介导免疫炎症的重要受体之一,它广泛分布于中枢神经系统。在胚胎早期,外源性或内源性配体激活TLRs,介导了一系列炎症反应,其产生的炎性因子对脑皮质发育有重大影响。因此,研究免疫炎症机制能为CD相关疾病的诊断、治疗及预防提供新思路。 | 马元施 刘仕勇 | 2017 | 医学综述2017，23，5： | 0 |
| 8 | Neurodevelopment and degeneration显示文摘Over the past decades,continuous effort has been made to resolve unsettled matters in the emerging scene of neuronal development.Despite the rapid progress,neuroscientists remain fascinated by the intricate networks of signaling pathways and molecules conserved | Margaret S.Ho | 2014 | Neuroscience Bulletin2014，30，4： | 0 |
| 9 | 神经系统SARM1条件性敲除小鼠的构建及其应用显示文摘目的:构建SARM1基因在神经细胞中条件性敲除小鼠模型,为探究SARM1基因在神经系统中的功能提供研究工具。方法:运用ES细胞打靶的方式构建SARM1^(flox/flox)转基因小鼠,并将其与表达Nestin-Cre重组酶的工具鼠进行杂交以产生神经元特异性SARM1基因敲除小鼠。然后使用PCR对敲除小鼠进行基因型鉴定,使用Western blot验证基因敲除效果。通过对小鼠进行旷场与高架十字迷宫试验来评估小鼠的情绪行为和焦虑水平。结果:SARM1蛋白主要表达于中枢神经系统,在神经元中高表达。PCR结果表明,成功构建了神经元特异性SARM1基因敲除小鼠。Western blot结果显示,与正常小鼠对比,SARM1^(Nestin)-CKO小鼠的脑组织中SARM1蛋白表达显著降低(P<0.05),并且SARM1基因敲除不影响小鼠的正常生长发育,也不影响脑组织的一般形态和神经细胞的数量。同时发现该条件性敲除小鼠不存在明显的焦虑样表型。结论:成功构建了SARM1基因在神经细胞中特异性敲除的小鼠动物模型,可为探讨SARM1基因在神经精神疾病中的作用提供重要研究平台。 | 项鲁丹 孙焕坤 吴仟 汪伟 黄智慧 于欣 | 2021 | 温州医科大学学报2021，51，4： | 0 |
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