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首页> 外文期刊>The European Journal of Neuroscience >Mitotic activity, modulation of DNA processing, and purinergic signalling in the adult rat auditory brainstem following sensory deafferentation
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Mitotic activity, modulation of DNA processing, and purinergic signalling in the adult rat auditory brainstem following sensory deafferentation

机译:在感官Deafferentation之后,在成年大鼠听觉脑干中,DNA处理的薄虫活性,DNA处理的调节和嘌呤能信号传导

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A complex scenario of cellular network reorganization is caused by unilateral sensory deafferentation (USD) in the adult rat central auditory system. We asked whether this plasticity response involves mitosis. Immunohistochemistry was applied to brainstem sections for the detection and localization of mitotic markers Ki67 and PCNA, the growth-associated protein Gap43 and purine receptor P2X4. Fluorescent double staining was done for Ki67:PCNA and for both of them with HuC/HuD (neurons), S100 (astrocytes), Iba1 (microglia) and P2X4. Inquiring 1-7 days after USD, we found Ki67 expression to be changed in cellular profiles of cochlear nucleus (CN) with a significant increase in number by 1-3 days, followed by reset to control level within 1 week. USD-induced mitosis exclusively occurred in microglia and was absent elsewhere in the auditory brainstem. PCNA staining of small cellular profiles increased similarly but remained elevated. PCNA staining intensity also changed in CN, superior olive and inferior colliculus in neuronal nuclei, suggesting shifts in DNA processing. No apoptotic cell death was detected in any region of the adult auditory brainstem after USD. A comparison of anterograde and retrograde effects of nerve damage revealed proliferating microglia expressing P2X4 receptors in CN upon USD, but not in the facial nucleus after facial nerve transection. In conclusion, the deafferentation model studied here permits insight into the capacity of the adult mammalian brain to invoke mitosis among glia cells, adjustment of gene processing in neurons and purinergic signalling between them, jointly accounting for a multilayered neuro- and glioplastic response.
机译:一种复杂的蜂窝网络重组场景是由成年大鼠中央听觉系统中单侧感官脱染(USD)引起的。我们询问这种可塑性反应是否涉及有丝分裂。将免疫组织化学应用于脑干分部,用于检测和定位有丝分裂标记Ki67和PC​​NA,生长相关蛋白质GAP43和嘌呤受体P2X4。为KI67:PCNA和HUC / HUD(神经元),S100(星形胶质细胞),IBA1(MICROGLIA)和P2X4进行荧光双染色。询问USD后1-7天,我们发现Ki67表达在耳蜗核(CN)的细胞谱中改变,数量大幅增加1-3天,然后在1周内重置控制水平。 USD诱导的有丝分裂在微胶质植物中发生,并且在听觉脑干中的其他地方缺席。小细胞谱的PCNA染色同样增加但保持升高。 PCNA染色强度也在CN,神经元细胞核中的CN,优质橄榄和劣质小集体中改变,表明DNA加工中的变化。在USD后,在成人听觉脑干的任何区域中没有检测到凋亡细胞死亡。神经损伤的逆行和逆行效应的比较显示CN在USD中CN中P2X4受体的增殖小胶质细胞,但在面神经横断后的面部核中。总之,研究的脱裂模型允许深入了解成人哺乳动物脑中的能力,以调节胶质细胞,在神经元和嘌呤能信号中调整它们之间的基因加工,共同核对多层神经和神经胶质反应。

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