Citation

Sabbagh JJ, Fontaine SN, Shelton LB, Blair LJ, Hunt JB, Zhang B, Lee DC, Lloyd JD, Dickey CA. J. Neurotrauma 2016; 33(19): 1751-1760.

Affiliation

James A. Haley Veteran's Hospital, Tampa, Florida, United States ; cdickey@health.usf.edu.

Copyright

(Copyright © 2016, Mary Ann Liebert Publishers)

DOI

10.1089/neu.2015.4288

PMID

26739819

Abstract

Traumatic brain injury (TBI) caused by improvised explosive devices (IEDs) is a growing problem in military settings, but modeling this disease in rodents to preclinically evaluate potential therapeutics has been challenging due to inconsistency between models. Although the effects of primary blast wave injury have been extensively studied, little is known regarding the effects of non-contact rotational head injuries independent of the blast wave. To model this type of injury, we generated an air cannon system that does not produce a blast wave, but generates enough air pressure to cause rotational head injury. Mice exposed to this type of injury showed deficits in cognitive and motor task acquisition within 1 to 2 weeks post-injury, but mice tested 7 to 8 weeks post-injury did not retain any deficits. This suggests that the effects of a single, non-contact rotational head injury are not long-lasting. Despite the transient nature of the behavioral deficits, increased levels of phosphorylated tau were observed at 2 and 8 weeks post-injury; however this tau did not adopt typical pathological structures that have been observed in other TBI models that incorporate blast waves. This was possibly due to the fact that this injury was insufficient to induce changes in microglial activation, which was not affected at 2 or 8 weeks post-injury. Taken together, these data suggest that exposure to non-contact, rotational head injury only produces transient cognitive anomalies, but elicits some minor lasting neuropathological changes.

Language: en