Graeber M B, Kreutzberg G W
Department of Neuromorphology, Max Planck Institute for Psychiatry, Martinsried-Munich, Federal Republic of Germany.
J Neurocytol. 1988 Apr;17(2):209-20. doi: 10.1007/BF01674208.
Transection of the facial nerve causes a rapid increase of glial fibrillary acidic protein in reactive astrocytes and a proliferation of local microglial cells. The latter is associated with a detachment of synaptic terminals from the regenerating motor neurons. About 3 weeks following axotomy the reactive astrocytes begin to form thin, sheet-like lamellar processes which cover virtually all neuronal surfaces. A high 5'-nucleotidase enzymic activity can be demonstrated in the plasma membrane of these thin cell processes. Subsequently, the lamellar processes become arranged in stacks which persist for several months and thus isolate the regenerating motor neurons from their afferent synaptic input. It is speculated that the process may protect the motor neurons during regeneration.
面神经横断会导致反应性星形胶质细胞中胶质纤维酸性蛋白迅速增加以及局部小胶质细胞增殖。后者与再生运动神经元突触终末的脱离有关。轴突切断后约3周，反应性星形胶质细胞开始形成薄的、片状的层状突起，几乎覆盖所有神经元表面。在这些薄细胞突起的质膜中可显示出高5'-核苷酸酶活性。随后，层状突起堆叠排列，持续数月，从而使再生运动神经元与其传入突触输入隔离。据推测，该过程可能在再生过程中保护运动神经元。
