Lagenaur C, Masters C, Schachner M
J Neurosci. 1982 Apr;2(4):470-6. doi: 10.1523/JNEUROSCI.02-04-00470.1982.
In response to mechanical injury in the adult mouse cerebellum, Bergmann glia and astrocytes of the granular layer exhibit abnormally increased expression of M1 antigen, while expression of C1 antigen in Bergmann glia is reduced. these reciprocal changes in two different astrocytic antigenic determinants (each recognized by monoclonal antibodies) are easily detected in the immediate area of the wound 4 days after the lesion. Although loss of C1 antigen from Bergmann glia remains localized to the area of the wound, abnormal M1 expression becomes widespread in cerebellar astrocytes, also affecting the contralateral side of the injured cerebellum at its peak 8 to 12 days after injury. These findings suggest that previous observations of abnormal expression of the two antigens in the cerebellum of mutant mice (Sommer, I., and M. Schachner (1981) J. Supramol. Struct. 16: 53-74) might be interpreted with the view that a glial reaction to pathological state might be induced by genetically programmed neuronal cell death and/or abnormal development. We therefore postulate that expression of M1 in astrocytes that normally do not express this antigen and repression of C1 in normally positive astrocytes are indicative of a distinct functional state of astroglia, reactive gliosis.
在成年小鼠小脑对机械损伤的反应中，伯格曼胶质细胞和颗粒层星形胶质细胞的M1抗原表达异常增加，而伯格曼胶质细胞中C1抗原的表达则降低。在损伤后4天，在伤口的直接区域很容易检测到这两种不同星形胶质细胞抗原决定簇（每种都由单克隆抗体识别）的这些相反变化。虽然伯格曼胶质细胞中C1抗原的缺失仍局限于伤口区域，但异常的M1表达在小脑星形胶质细胞中变得广泛，在损伤后8至12天达到峰值时也影响受伤小脑的对侧。这些发现表明，先前在突变小鼠小脑中观察到的两种抗原的异常表达（Sommer, I., and M. Schachner (1981) J. Supramol. Struct. 16: 53 - 74），可能可以解释为一种观点，即对病理状态的胶质细胞反应可能是由基因编程的神经元细胞死亡和/或异常发育诱导的。因此，我们推测，在正常情况下不表达该抗原的星形胶质细胞中M1的表达以及在正常呈阳性的星形胶质细胞中C1的抑制，表明了星形胶质细胞的一种独特功能状态，即反应性胶质增生。
