TY  - JOUR
PY  - 2016//
TI  - Primary blast injury causes cognitive impairments and hippocampal circuit alterations
JO  - Experimental neurology
A1  - Beamer, Matthew
A1  - Tummala, Shanti R.
A1  - Gullotti, David
A1  - Kopil, Catherine
A1  - Gorka, Samuel
A1  - Ted Abel, 
A1  - Bass, Cameron R. Dale
A1  - Morrison, Barclay
A1  - Cohen, Akiva S.
A1  - Meaney, David F.
SP  - 16
EP  - 28
VL  - 283
IS  - Pt A
N2  - Blast-induced traumatic brain injury (bTBI) and its longterm consequences are a major health concern among veterans. Despite recent work enhancing our knowledge about bTBI, very little is known about the contribution of the blast wave alone to the observed sequelae. Herein, we isolated its contribution in a mouse model by constraining the animals' heads during exposure to a shockwave (primary blast). Our results show that exposure to primary blast alone results in changes in hippocampus-dependent behaviors that correspond with electrophysiological changes in area CA1 and are accompanied by reactive gliosis. Specifically, five days after exposure, behavior in an open field and performance in a spatial object recognition (SOR) task were significantly different from sham. Network electrophysiology, also performed five days after injury, demonstrated a significant decrease in excitability and increase in inhibitory tone. Immunohistochemistry for GFAP and Iba1 performed ten days after injury showed a significant increase in staining. Interestingly, a threefold increase in the impulse of the primary blast wave did not exacerbate these measures. However, we observed a significant reduction in the contribution of the NMDA receptors to the field EPSP at the highest blast exposure level. Our results emphasize the need to account for the effects of primary blast loading when studying the sequelae of bTBI.<br><br>Copyright © 2015. Published by Elsevier Inc.<p />  <p>Language: en</p>
LA  - en
SN  - 0014-4886
UR  - http://dx.doi.org/10.1016/j.expneurol.2016.05.025
ID  - ref1
ER  -