Temporal assessment of traumatic axonal injury in the rat corpus callosum and optic chiasm

Abstract

Impaired axoplasmic transport (IAT) and neurofilament compaction (NFC), two common axonal pathology processes involved in traumatic axonal injury (TAI), have been well characterized. TAI is found clinically and in animal models in brainstem white matter (WM) tracts and in the corpus callosum (CC), optic chiasm (Och), and internal capsule. Previous published quantitative studies of the time course of TAI expression induced by the Marmarou impact acceleration model have been limited to the brainstem. Accordingly, this study assessed the extent of IAT and NFC in the CC and Och at 8h, 28 h, 3 days and 7 days after traumatic brain injury (TBI) induction by the Marmarou impact acceleration model. IAT peak density was observed at 8h in the CC and 28 h in the Och post-TBI. NFC peak density was observed at 28 h in both structures. The density of IAT and NFC decreased with increasing survival time in both structures. The NFC density time profile followed a similar trend in both the Och and CC, whereas the IAT density time profile was variable between the Och and CC. Furthermore, a strong linear relationship was observed between IAT and NFC in the CC but not in the Och. These findings highlight the heterogeneity of TAI as evidenced by variable IAT and NFC injury time profiles in each anatomical structure. This variability indicates the requirement of multiple markers for a comprehensive TAI evaluation and multiple targeted treatments for TAI polypathology within its therapeutic window time frame.