Impaired axoplasmic transport is the dominant injury induced by an impact acceleration injury device: an analysis of traumatic axonal injury in pyramidal tract and corpus callosum of rats.

Traumatic axonal injury (TAI) involves neurofilament compaction (NFC) and impaired axoplasmic transport (IAT) in distinct populations of axons. Previous quantification studies of TAI focused on limited areas of pyramidal tract (Py) but not its entire length. Quantification of TAI in corpus callosum (CC) and its comparison to that in Py is also lacking. This study assessed and compared the extent of TAI in the entire Py and CC of rats following TBI. TBI was induced by a modified Marmarou impact acceleration device in 31 adult male Sprague Dawley rats by dropping a 450 gram impactor from either 1.25 m or 2.25 m. Twenty-four hours after TBI, TAI was assessed by beta amyloid precursor protein (β-APP-IAT) and RMO14 (NFC) immunocytochemistry. TAI density (β-APP and RMO14 axonal swellings, retraction balls and axonal profiles) was counted from panoramic images of CC and Py. Significantly high TAI was observed in 2.25 m impacted rats. β-APP immunoreactive axons were significantly higher in number than RMO14 immunoreactive axons in both the structures. TAI density in Py was significantly higher than in CC. Based on our parallel biomechanical studies, it is inferred that TAI in CC may be related to compressive strains and that in Py may be related to tensile strains. Overall, IAT appears to be the dominant injury type induced by this model and injury in Py predominates that in CC.