PMID- 27246999
OWN - NLM
STAT- MEDLINE
DCOM- 20170505
LR  - 20220321
IS  - 1090-2430 (Electronic)
IS  - 0014-4886 (Print)
IS  - 0014-4886 (Linking)
VI  - 283
IP  - Pt A
DP  - 2016 Sep
TI  - Primary blast injury causes cognitive impairments and hippocampal circuit 
      alterations.
PG  - 16-28
LID - S0014-4886(16)30143-1 [pii]
LID - 10.1016/j.expneurol.2016.05.025 [doi]
AB  - 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.
CI  - Copyright (c) 2016. Published by Elsevier Inc.
FAU - Beamer, Matthew
AU  - Beamer M
AD  - Department of Bioengineering(1), University of Pennsylvania, Philadelphia, PA, 
      USA.
FAU - Tummala, Shanti R
AU  - Tummala SR
AD  - Department of Bioengineering(1), University of Pennsylvania, Philadelphia, PA, 
      USA.
FAU - Gullotti, David
AU  - Gullotti D
AD  - Department of Bioengineering(1), University of Pennsylvania, Philadelphia, PA, 
      USA.
FAU - Kopil, Catherine
AU  - Kopil C
AD  - Department of Bioengineering(1), University of Pennsylvania, Philadelphia, PA, 
      USA.
FAU - Gorka, Samuel
AU  - Gorka S
AD  - Department of Bioengineering(1), University of Pennsylvania, Philadelphia, PA, 
      USA.
FAU - Ted Abel
AU  - Ted Abel
AD  - Department of Biology, University of Pennsylvania, Philadelphia, PA, USA.
FAU - Bass, Cameron R Dale
AU  - Bass CR
AD  - Department of Biomedical Engineering, Duke University, Durham, NC, USA.
FAU - Morrison, Barclay 3rd
AU  - Morrison B 3rd
AD  - Department of Biomedical Engineering, Columbia University, New York, NY, USA.
FAU - Cohen, Akiva S
AU  - Cohen AS
AD  - Department of Anesthesiology and Critical Care Medicine, University of 
      Pennsylvania, Philadelphia, PA, USA; Division of Critical Care Medicine, 
      Children's Hospital of Philadelphia, Philadelphia, PA, USA.
FAU - Meaney, David F
AU  - Meaney DF
AD  - Department of Bioengineering(1), University of Pennsylvania, Philadelphia, PA, 
      USA; Department of Neurosurgery, University of Pennsylvania, Philadelphia, PA, 
      USA. Electronic address: dmeaney@seas.upenn.edu.
LA  - eng
GR  - R01 NS045975/NS/NINDS NIH HHS/United States
GR  - R01 NS069629/NS/NINDS NIH HHS/United States
GR  - R01 NS088176/NS/NINDS NIH HHS/United States
GR  - R37 HD059288/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20160528
PL  - United States
TA  - Exp Neurol
JT  - Experimental neurology
JID - 0370712
RN  - 0 (Aif1 protein, mouse)
RN  - 0 (Calcium-Binding Proteins)
RN  - 0 (Excitatory Amino Acid Antagonists)
RN  - 0 (Glial Fibrillary Acidic Protein)
RN  - 0 (Microfilament Proteins)
RN  - 6OTE87SCCW (6-Cyano-7-nitroquinoxaline-2,3-dione)
SB  - IM
MH  - 6-Cyano-7-nitroquinoxaline-2,3-dione/pharmacology
MH  - Animals
MH  - Biomechanical Phenomena
MH  - Brain Injuries/*complications/*pathology
MH  - Calcium-Binding Proteins/metabolism
MH  - Cognition Disorders/*etiology
MH  - Disease Models, Animal
MH  - Excitatory Amino Acid Antagonists/pharmacology
MH  - Exploratory Behavior/physiology
MH  - Fear/psychology
MH  - Glial Fibrillary Acidic Protein/metabolism
MH  - Hippocampus/*pathology
MH  - Male
MH  - Maze Learning
MH  - Membrane Potentials/drug effects
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Microfilament Proteins/metabolism
MH  - Motor Activity/physiology
MH  - Nerve Net/*pathology
MH  - Rotarod Performance Test
MH  - Time Factors
PMC - PMC5062598
MID - NIHMS795917
OTO - NOTNLM
OT  - Blast induced traumatic brain injury
OT  - Blood-brain barrier
OT  - Concussion
EDAT- 2016/06/02 06:00
MHDA- 2017/05/06 06:00
PMCR- 2016/10/13
CRDT- 2016/06/02 06:00
PHST- 2016/01/22 00:00 [received]
PHST- 2016/05/14 00:00 [revised]
PHST- 2016/05/20 00:00 [accepted]
PHST- 2016/06/02 06:00 [entrez]
PHST- 2016/06/02 06:00 [pubmed]
PHST- 2017/05/06 06:00 [medline]
PHST- 2016/10/13 00:00 [pmc-release]
AID - S0014-4886(16)30143-1 [pii]
AID - 10.1016/j.expneurol.2016.05.025 [doi]
PST - ppublish
SO  - Exp Neurol. 2016 Sep;283(Pt A):16-28. doi: 10.1016/j.expneurol.2016.05.025. Epub 
      2016 May 28.