PMID- 12477627
OWN - NLM
STAT- MEDLINE
DCOM- 20030128
LR  - 20190901
IS  - 0379-0738 (Print)
IS  - 0379-0738 (Linking)
VI  - 130
IP  - 2-3
DP  - 2002 Dec 4
TI  - The expression of excitatory amino acid transporter 2 in traumatic brain injury.
PG  - 83-9
AB  - It is well recognized that glutamate is the major excitatory neurotransmitter, 
      which is removed from the synaptic cleft by excitatory amino acid transporter 2 
      (EAAT2) located on the perisynaptic astrocytes and that neuronal death has been 
      associated with an increased extracellular glutamate concentration. In this 
      study, we have immunohistochemically demonstrated the expression of EAAT2 protein 
      in the human brain after traumatic brain injury (TBI). The EAAT2 expression 
      patterns can be divided into three types: continuous and highly extensive 
      staining (E); continuous but sporadic staining (M); and sporadic pattern staining 
      (S). In six of the nine short survival cases studied (1 h to 1 day), continuous 
      and highly extensive staining for EAAT2 (E type) was observed in the ipsilateral 
      cerebral cortex. On the other hand, we were able to demonstrate weak staining (S 
      and M types) in 5 of the 7 long survival cases (> or =1 day) and in 12 of the 14 
      very short survival cases (<1 h) studied. Similar findings were obtained in the 
      contralateral cerebral cortex and also in the ipsilateral hippocampus. In 
      addition, positive staining for glial fibrillary acidic protein was detected 
      around the cerebral contusion, but the EAAT2-positive expression was not observed 
      in the same region for all of the six short and long survival cases (> or =1 h) 
      after TBI. These findings clearly showed the differences in EAAT2 expression in 
      the cerebral cortex according to the survival time and severity of cerebral 
      contusion after TBI. Therefore, we emphasized that EAAT2 might play an important 
      role in contributing to extracellular glutamate concentrations and secondary 
      brain injury after TBI.
CI  - Copyright 2002 Elsevier Science Ireland Ltd.
FAU - Ikematsu, Kazuya
AU  - Ikematsu K
AD  - Division of Forensic Pathology and Science, Department of Translational Medical 
      Sciences, Course of Medical and Dental Sciences, Graduate School of Biochemical 
      Sciences, Nagasaki University, 1-12-4 Sakamoto, Nagasaki 852-8523, Japan.
FAU - Tsuda, Ryouichi
AU  - Tsuda R
FAU - Kondo, Toshikazu
AU  - Kondo T
FAU - Nakasono, Ichiro
AU  - Nakasono I
LA  - eng
PT  - Journal Article
PL  - Ireland
TA  - Forensic Sci Int
JT  - Forensic science international
JID - 7902034
RN  - 0 (Excitatory Amino Acids)
RN  - 0 (Glial Fibrillary Acidic Protein)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Autopsy
MH  - Brain Injuries/*metabolism
MH  - Case-Control Studies
MH  - Cerebral Cortex/*metabolism
MH  - Child
MH  - Child, Preschool
MH  - Excitatory Amino Acids/*metabolism
MH  - Female
MH  - Forensic Medicine/methods
MH  - Glial Fibrillary Acidic Protein/metabolism
MH  - Hippocampus/metabolism
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Time Factors
EDAT- 2002/12/13 04:00
MHDA- 2003/01/29 04:00
CRDT- 2002/12/13 04:00
PHST- 2002/12/13 04:00 [pubmed]
PHST- 2003/01/29 04:00 [medline]
PHST- 2002/12/13 04:00 [entrez]
AID - S0379073802003444 [pii]
AID - 10.1016/s0379-0738(02)00344-4 [doi]
PST - ppublish
SO  - Forensic Sci Int. 2002 Dec 4;130(2-3):83-9. doi: 10.1016/s0379-0738(02)00344-4.