PMID- 27573357
OWN - NLM
STAT- MEDLINE
DCOM- 20180301
LR  - 20190111
IS  - 1557-9042 (Electronic)
IS  - 0897-7151 (Linking)
VI  - 34
IP  - 5
DP  - 2017 Mar 1
TI  - Primary Blast Injury Depressed Hippocampal Long-Term Potentiation through 
      Disruption of Synaptic Proteins.
PG  - 1063-1073
LID - 10.1089/neu.2016.4578 [doi]
AB  - Blast-induced traumatic brain injury (bTBI) is a major threat to United States 
      service members in military conflicts worldwide. The effects of primary blast, 
      caused by the supersonic shockwave interacting with the skull and brain, remain 
      unclear. Our group has previously reported that in vitro primary blast exposure 
      can reduce long-term potentiation (LTP), the electrophysiological correlate of 
      learning and memory, in rat organotypic hippocampal slice cultures (OHSCs) 
      without significant changes to cell viability or basal, evoked neuronal function. 
      We investigated the time course of primary blast-induced deficits in LTP and the 
      molecular mechanisms that could underlie these deficits. We found that pure 
      primary blast exposure induced LTP deficits in a delayed manner, requiring longer 
      than 1 hour to develop, and that these deficits spontaneously recovered by 10 
      days following exposure depending on blast intensity. Additionally, we observed 
      that primary blast exposure reduced total 
      alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamate receptor 1 
      (GluR1) subunit expression and phosphorylation of the GluR1 subunit at the 
      serine-831 site. Blast also reduced the expression of postsynaptic density 
      protein-95 (PSD-95) and phosphorylation of stargazin protein at the 
      serine-239/240 site. Finally, we found that modulation of the cyclic adenosine 
      monophosphate (cAMP) pathway ameliorated electrophysiological and 
      protein-expression changes caused by blast. These findings could inform the 
      development of novel therapies to treat blast-induced loss of neuronal function.
FAU - Vogel, Edward W 3rd
AU  - Vogel EW 3rd
AD  - 1 Department of Biomedical Engineering, Columbia University , New York, New York.
FAU - Rwema, Steve H
AU  - Rwema SH
AD  - 1 Department of Biomedical Engineering, Columbia University , New York, New York.
FAU - Meaney, David F
AU  - Meaney DF
AD  - 2 Department of Bioengineering, University of Pennsylvania , Philadelphia, 
      Pennsylvania.
FAU - Bass, Cameron R Dale
AU  - Bass CR
AD  - 3 Department of Biomedical Engineering, Duke University , Durham, North Carolina.
FAU - Morrison, Barclay 3rd
AU  - Morrison B 3rd
AD  - 1 Department of Biomedical Engineering, Columbia University , New York, New York.
LA  - eng
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20161013
PL  - United States
TA  - J Neurotrauma
JT  - Journal of neurotrauma
JID - 8811626
RN  - 0 (Cacng2 protein, rat)
RN  - 0 (Calcium Channels)
RN  - 0 (Disks Large Homolog 4 Protein)
RN  - 0 (Dlg4 protein, rat)
RN  - 0 (Receptors, AMPA)
RN  - E0399OZS9N (Cyclic AMP)
RN  - TFZ3H25BS1 (glutamate receptor ionotropic, AMPA 1)
SB  - IM
MH  - Animals
MH  - Blast Injuries/*complications
MH  - Brain Injuries, Traumatic/etiology/*metabolism/*physiopathology
MH  - Calcium Channels/metabolism
MH  - Cyclic AMP/metabolism
MH  - Disease Models, Animal
MH  - Disks Large Homolog 4 Protein/metabolism
MH  - Hippocampus/*metabolism/*physiopathology
MH  - Long-Term Potentiation/*physiology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, AMPA/metabolism
MH  - Signal Transduction/physiology
MH  - Synapses/*metabolism
OTO - NOTNLM
OT  - TBI
OT  - electrophysiology
OT  - in vitro studies
OT  - learning and memory
OT  - military injury
EDAT- 2016/08/31 06:00
MHDA- 2018/03/02 06:00
CRDT- 2016/08/31 06:00
PHST- 2016/08/31 06:00 [pubmed]
PHST- 2018/03/02 06:00 [medline]
PHST- 2016/08/31 06:00 [entrez]
AID - 10.1089/neu.2016.4578 [doi]
PST - ppublish
SO  - J Neurotrauma. 2017 Mar 1;34(5):1063-1073. doi: 10.1089/neu.2016.4578. Epub 2016 
      Oct 13.