TY - JOUR
T1 - Noncontact Rotational Head Injury Produces Transient Cognitive Deficits but Lasting Neuropathological Changes
AU - Sabbagh, Jonathan J.
AU - Fontaine, Sarah N.
AU - Shelton, Lindsey B.
AU - Blair, Laura J.
AU - Hunt, Jerry B.
AU - Zhang, Bo
AU - Gutmann, Joseph M.
AU - Lee, Daniel C.
AU - Lloyd, John D.
AU - Dickey, Chad A.
N1 - Publisher Copyright:
Copyright © 2016, Mary Ann Liebert, Inc.
Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 2016/10/1
Y1 - 2016/10/1
N2 - Traumatic brain injury (TBI) caused by improvised explosive devices (IEDs) is a growing problem in military settings, but modeling this disease in rodents to pre-clinically evaluate potential therapeutics has been challenging because of inconsistency between models. Although the effects of primary blast wave injury have been extensively studied, little is known regarding the effects of noncontact rotational TBIs 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 TBI. Mice exposed to this type of injury showed deficits in cognitive and motor task acquisition within 1-2 weeks post-injury, but mice tested 7-8 weeks post-injury did not retain any deficits. This suggests that the effects of a single, noncontact rotational TBI 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 attributed 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 noncontact, rotational head injury only produces transient cognitive anomalies, but elicits some minor lasting neuropathological changes.
AB - Traumatic brain injury (TBI) caused by improvised explosive devices (IEDs) is a growing problem in military settings, but modeling this disease in rodents to pre-clinically evaluate potential therapeutics has been challenging because of inconsistency between models. Although the effects of primary blast wave injury have been extensively studied, little is known regarding the effects of noncontact rotational TBIs 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 TBI. Mice exposed to this type of injury showed deficits in cognitive and motor task acquisition within 1-2 weeks post-injury, but mice tested 7-8 weeks post-injury did not retain any deficits. This suggests that the effects of a single, noncontact rotational TBI 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 attributed 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 noncontact, rotational head injury only produces transient cognitive anomalies, but elicits some minor lasting neuropathological changes.
KW - animal studies
KW - learning and memory
KW - traumatic brain injury
UR - http://www.scopus.com/inward/record.url?scp=84990050231&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84990050231&partnerID=8YFLogxK
U2 - 10.1089/neu.2015.4288
DO - 10.1089/neu.2015.4288
M3 - Article
AN - SCOPUS:84990050231
SN - 0897-7151
VL - 33
SP - 1751
EP - 1760
JO - Journal of Neurotrauma
JF - Journal of Neurotrauma
IS - 19
ER -