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抗血清诱导的体外髓鞘形成解离:一项超微结构研究

Antiserum-induced dissociation of myelinogenesis in vitro. An ultrastructural study.

作者信息

Raine C S, Diaz M, Pakingan M, Bornstein M B

出版信息

Lab Invest. 1978 Apr;38(4):397-403.

PMID:642450
Abstract

Mature, myelinated cultures of mouse spinal cord tissue exposed to heated (decomplemented) sera from animals suffering from experimental allergic encephalomyelitis demonstrate a unique pattern of myelin swelling without demyelination. In the present study, three concentrations of heated experimental allergic encephalomyelitis sera (5, 15, and 25 per cent) were applied to spinal cord cultures from the time of explantation and continued for 33 days therafter. The sera were obtained from rabbits with the exposed cultures, glial cell differentiation occurred at timepoints comparable to those in normal unexposed sister cultures. Oligodendroglia produced a profusion of cytoplasmic processes which compacted to form aberrant myelin with a periodicity double that of normal myelin, containing four leaflets in the position of the normally bilamellar intraperiod line. The degree of the oligodendroglial abnormality was dose dependent, 25 per cent heated experimental allergic encephalomyelitis serum being the most potent. Frequently, in older cultures, large diameter axons, which under normal circumstances would have been well myelinated, were devoid of myelin sheaths although abundant aberrant myelin could be seen around nearby oligodendroglial cells. Rarely similar aberrant myelin was deposited around axons. It appeared, therefore, that the oligodendroglial cells had proliferated myelin which was unable to reach axons, possibly reflecting a failure in recognition between the two.

摘要

将来自患有实验性变应性脑脊髓炎动物的加热(灭活补体)血清,作用于成熟的、有髓鞘的小鼠脊髓组织培养物,会呈现出一种独特的髓鞘肿胀模式,而不会发生脱髓鞘。在本研究中,从接种时起,将三种浓度(5%、15%和25%)的加热实验性变应性脑脊髓炎血清应用于脊髓培养物,并在之后持续33天。血清取自兔子,对于暴露的培养物,神经胶质细胞分化发生的时间点与正常未暴露的姐妹培养物相当。少突胶质细胞产生大量胞质突起,这些突起聚集形成异常髓鞘,其周期是正常髓鞘的两倍,在正常双板层内节线的位置含有四个板层。少突胶质细胞异常的程度呈剂量依赖性,25%加热实验性变应性脑脊髓炎血清最为有效。在较老的培养物中,通常情况下本应被良好髓鞘化的大直径轴突常常没有髓鞘,尽管在附近的少突胶质细胞周围可以看到大量异常髓鞘。很少有类似的异常髓鞘沉积在轴突周围。因此,似乎少突胶质细胞增殖产生了无法到达轴突的髓鞘,这可能反映了两者之间识别的失败。

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