PMID- 24978397
OWN - NLM
STAT- MEDLINE
DCOM- 20150224
LR  - 20140709
IS  - 1473-558X (Electronic)
IS  - 0959-4965 (Linking)
VI  - 25
IP  - 12
DP  - 2014 Aug 20
TI  - Hippocampal immediate early gene transcription in the rat fluid percussion 
      traumatic brain injury model.
PG  - 954-9
LID - 10.1097/WNR.0000000000000219 [doi]
AB  - Traumatic brain injury (TBI) is one of the leading causes of neurological 
      disability and death in the USA across all age groups, ethnicities, and incomes. 
      In addition to the short-term morbidity and mortality, TBI leads to epilepsy and 
      severe neurocognitive symptoms, both of which are referenced to post-traumatic 
      hippocampal dysfunction, although the mechanisms of such hippocampal dysfunction 
      are incompletely understood. Here, we study the temporal profile of the 
      transcription of three select immediate early gene (IEG) markers of neuronal 
      hyperactivation, plasticity, and injury, c-fos, brain-derived neurotrophic factor 
      (BDNF), and Bax, in the acute period following the epileptogenic lateral fluid 
      percussion injury in a rodent TBI model. We found that lateral fluid percussion 
      injury leads to enhanced expression of the selected IEGs within 24 h of TBI. 
      Specifically, BDNF and c-fos increase maximally 1-6 h after TBI in the 
      ipsilesional hippocampus, whereas Bax increases in the hippocampus bilaterally in 
      this time window. Antagonism of the N-methyl-D-aspartate-type glutamate receptor 
      by MK801 attenuates the increase in BDNF and Bax, which underscores a therapeutic 
      role for N-methyl-D-aspartate-type glutamate receptor antagonism in the acute 
      post-traumatic time period and suggests a value to a hippocampal IEG readout as 
      an outcome after injury or acute therapeutic intervention.
FAU - Wang, Yingpeng
AU  - Wang Y
AD  - Departments of aNeurology bNeurosurgery, Boston Children's Hospital, Harvard 
      Medical School, Boston, Massachusetts cDepartment of Neurology, University of 
      Chicago, Chicago, Illinois, USA dDepartment of Neurology, Beijing Aerospace 
      General Hospital eCenter for Infectious Diseases, Beijing You'an Hospital, 
      Capital Medical University, Beijing, China.
FAU - Hameed, Mustafa Q
AU  - Hameed MQ
FAU - Rakhade, Sanjay N
AU  - Rakhade SN
FAU - Iglesias, Antonio H
AU  - Iglesias AH
FAU - Muller, Paul A
AU  - Muller PA
FAU - Mou, Dan-Lei
AU  - Mou DL
FAU - Rotenberg, Alexander
AU  - Rotenberg A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - England
TA  - Neuroreport
JT  - Neuroreport
JID - 9100935
RN  - 0 (Bax protein, rat)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Excitatory Amino Acid Antagonists)
RN  - 0 (Proto-Oncogene Proteins c-fos)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 0 (bcl-2-Associated X Protein)
RN  - 6LR8C1B66Q (Dizocilpine Maleate)
SB  - IM
MH  - Acute Disease
MH  - Animals
MH  - Brain Injuries/drug therapy/*metabolism
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Disease Models, Animal
MH  - Dizocilpine Maleate/pharmacology
MH  - Excitatory Amino Acid Antagonists/pharmacology
MH  - Functional Laterality
MH  - Hippocampus/drug effects/*metabolism
MH  - Male
MH  - Proto-Oncogene Proteins c-fos/*metabolism
MH  - RNA, Messenger/metabolism
MH  - Rats, Long-Evans
MH  - Real-Time Polymerase Chain Reaction
MH  - Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/metabolism
MH  - Time Factors
MH  - Transcription, Genetic/drug effects
MH  - bcl-2-Associated X Protein/*metabolism
EDAT- 2014/07/01 06:00
MHDA- 2015/02/25 06:00
CRDT- 2014/07/01 06:00
PHST- 2014/07/01 06:00 [entrez]
PHST- 2014/07/01 06:00 [pubmed]
PHST- 2015/02/25 06:00 [medline]
AID - 10.1097/WNR.0000000000000219 [doi]
PST - ppublish
SO  - Neuroreport. 2014 Aug 20;25(12):954-9. doi: 10.1097/WNR.0000000000000219.