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神经元吞噬细胞引起的免疫相关抗原表达改变并不能改善大鼠面神经严重损伤后的神经元存活情况。

Altered expression of immune-related antigens by neuronophages does not improve neuronal survival after severe lesion of the facial nerve in rats.

作者信息

Angelov D N, Krebs C, Walther M, Martinez-Portillo F J, Gunkel A, Lay C H, Streppel M, Guntinas-Lichius O, Stennert E, Neiss W F

机构信息

Institut I für Anatomie, Universität zu Köln, Germany.

出版信息

Glia. 1998 Oct;24(2):155-71.

PMID:9728762
Abstract

Injection of Fluoro-Gold (FG) into the whiskerpad muscles of rats yields a permanent retrograde labeling of motoneurons in the facial nucleus. Following subsequent resection of 10 mm of the facial nerve, one-third of the facial motoneurons die and the microglia phagocytize the dead FG-labeled neurons, take up FG, and get labeled in vivo. The resulting identification of all FG-labeled cells allows long-term comparative investigations on the behavior of neuronophages. In this study, we used two groups of rats to test whether the quantified expression of five immune-related antigens by neuronophages was related to quantified decline in neuron number (counts after immunostaining for neuron-specific enolase) 3 to 224 days after resection of the facial nerve. Rats of the first group received standard food and those of the second group, pellets containing 1,000 ppm of the calcium channel blocker nimodipine. Image analysis of the number of FG-containing cells and the number and projection area of immunopositive neuronophages in serial sections for each antigen showed that nimodipine significantly attenuated the immunostaining for CR3, MHC class I, and class II antigens (monoclonal antibodies [MAbs] OX-42, OX-18, and OX-6); enhanced the expression of monocyte-macrophage-specific antigen (MAb ED1); and did not change the expression of rat macrophage differentiation antigen (MAb ED2). The altered expressions, however, had no effect on the loss of motoneurons in the lesioned facial nucleus. We conclude that the degree of expression of immune-related antigens by neuronophages has no influence on the delayed neuronal cell death induced by permanent target deprivation.

摘要

向大鼠的触须垫肌肉注射荧光金(FG)可对面神经核中的运动神经元进行永久性逆行标记。在随后切除10毫米面神经后,三分之一的面神经运动神经元死亡,小胶质细胞吞噬死亡的FG标记神经元,摄取FG,并在体内被标记。对所有FG标记细胞的鉴定使得能够对噬神经元细胞的行为进行长期比较研究。在本研究中,我们使用两组大鼠来测试噬神经元细胞对五种免疫相关抗原的定量表达是否与面神经切除后3至224天神经元数量的定量下降(神经元特异性烯醇化酶免疫染色后的计数)有关。第一组大鼠给予标准食物,第二组大鼠给予含有1000 ppm钙通道阻滞剂尼莫地平的颗粒饲料。对每个抗原的连续切片中含FG细胞的数量以及免疫阳性噬神经元细胞的数量和投射面积进行图像分析表明,尼莫地平显著减弱了CR3、MHC I类和II类抗原(单克隆抗体[MAb]OX-42、OX-18和OX-6)的免疫染色;增强了单核细胞-巨噬细胞特异性抗原(MAb ED1)的表达;并且没有改变大鼠巨噬细胞分化抗原(MAb ED2)的表达。然而,这些改变的表达对损伤面神经核中运动神经元的丧失没有影响。我们得出结论,噬神经元细胞对免疫相关抗原的表达程度对永久性靶剥夺诱导的延迟性神经元细胞死亡没有影响。

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