a role of glial cells in the central nervous system to prevent retrograde degeneration of the facial nucleus and a mechanism for axonal regeneration

利用从脑干到靶点的全面神经轴突损伤模型，分析运动神经元逆行变性的机制，寻求神经元丧失的预防因素。外周损伤引起的运动神经元变性很小，而脑干损伤则表现为大量快速变性，导致28天仅3%的神经元存活。自体周围神经移植可诱导轴突存活8倍，促红细胞生成素3倍，但未发现其他神经保护因子。一氧化氮被认为与神经元丢失的机制有关，但与细胞凋亡的机制无关。逆行性变性的神经保护机制可能给我们中枢神经系统再生的线索。

Axonal injury models throughout the facial nerve from brainstem to the target was utilized to analyze the mechanism of retrograde motoneuron degeneration and seek the preventing factors against the neuronal loss. Peripheral injury induced little motoneuron degeneration, but brainstem injury showed massive and rapid degeneration resulting in only 3% neuronal survival on day 28.Peripheral nerve autograft induced 8-times axonal survival and erythropoietin 3-times, but no other neuroprotective factors found so far. Nitric oxide was supposed to be related to the mechanism of neuronal loss but apoptosis was not. The neuroprotective mechanism for retrograde degeneration might give us the cue for CNS regeneration.