| Summary: | 碩士 === 國立臺灣大學 === 解剖學研究所 === 93 === To understand the role of NO and free radical environment on the survival of periphery-projection central neurons following axonal injury, we studied the temporal expressions of four free radical enzymes, the severity of cell loss, the perineuronal astrocytic and microglial reactions, and the degeneration of the proximal central axons of facial motoneurons following close and distant axotomies at the brainstem surface and stylomastoid foramen, respectively. Distant lesion upregulated NOS, persistently downregulated the NOS-activating enzyme calcineurin, transiently upregulated the Mn-SOD expressions of these neurons, and resulted in mild neuron loss. On the other hand, close lesion upregulated NOS but downregulated calcineurin transiently and Mn-SOD expression specifically at 4-week-post-injury. This led to severe cell loss and neurons were found to contain swollen mitochondria 2–4 weeks postinjury. Neither nuclear fragmentation nor TUNEL reactivity was identified. This suggests that downregulation of Mn-SOD expression and the subsequent mitochondrial free radical toxicity are likely to be responsible for the death of axotomized periphery-projection central neurons. Close axotomy caused an earlier transformation of reactive glial morphologies, including the hypertrophy of astrocytic processes and metamorphosis of ramified microglia to amoeboid cells, than distant injury. Unlike rubrospinal neurons whose central axons degenerated slowly and anterogradely only following the severe loss of cell bodies elicited by close axotomy, the central axons of facial motoneurons degenerated quickly and retrogradely independent of the severity of their cell body loss. This shows that although central neurons projecting within and outside the CNS have cell bodies, dendrites and part of their axons in the same CNS environment, they are inheritably different and react differently to axonal injuries.
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