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Primary blast injury causes cognitive impairments and hippocampal circuit alterations
Journal article   Peer reviewed

Primary blast injury causes cognitive impairments and hippocampal circuit alterations

Matthew Beamer, Shanti R Tummala, David Gullotti, Catherine Kopil, Samuel Gorka, Ted Abel, Cameron R. “Dale” Bass, Barclay Morrison, Akiva S Cohen and David F Meaney
Experimental neurology, Vol.283(Pt A), pp.16-28
09/2016
DOI: 10.1016/j.expneurol.2016.05.025
PMCID: PMC5062598
PMID: 27246999

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Abstract

Blast-induced traumatic brain injury (bTBI) and its long term 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. •The effects of a primary blast load applied on the mouse brain are isolated.•Performance in a spatial object recognition task and open field is impaired.•Network excitability in area CA1 is decreased and inhibition is augmented.•Increased gliosis (GFAP and Iba1 staining) appear in the hippocampus.•Blast induced changes in brain function were independent of overpressure.
Blood-Brain Barrier Concussion Blast induced traumatic brain injury

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