Wallerian degeneration (WaD), commonly secondary to cerebral infarction, is the descending damage of fiber tracts with their accompanying myelin sheaths. However, whether this sequential injury can occur in non-ischemic corpus callosum (CC) and striatum in focal cortical ischemic model has not been fully demonstrated. The present study aimed to elucidate detailed histopathologic changes in CC and striatum after acute focal cortical infarction induced by permanent distal middle cerebral artery occlusion (dMCAO) in Sprague-Dawley rat. We found that myelin integrity, myelin-related proteins, MBP and MAG, and NF200-marked neurofilaments were all compromised in non-ischemic white matter regions, bilateral CC and ipsilateral striatum, along with cortical ischemia (all P < 0.05). Electron microscopy showed wide gaps between myelin sheath layers or between axon and myelin, with an abnormal folding of myelin sheath, and enlarged fluid-filled areas. APP accumulations were noted at 24 h post-dMCAO in those non-ischemic regions, and the deposition prolonged until 14 days after cortical ischemia (all P < 0.05). Moreover, in these areas, microglia and astrocytes were robustly and persistently activated in different patterns. No substantial changes were observed in contralateral striatum. In conclusion, our results suggest that WaD may be involved in non-ischemic CC and striatum after focal cortical infarction, accompanied by APP aggregation and neuroglia initiation forming the glial scar.
Keywords: Demyelination; Distal middle cerebral artery occlusion (dMCAO); Glial cells; Wallerian degeneration.
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