Changes in glial glutamate transporters in human epileptogenic hippocampus: Inadequate explanation for high extracellular glutamate during seizures

Abstract Temporal lobe epilepsy (TLE) with hippocampal sclerosis is associated with high extracellular glutamate levels, which could trigger seizures. Down-regulation of glial glutamate transporters GLAST (EAAT1) and GLT-1 (EAAT2) in sclerotic hippocampi may account for such increases. Their distrib...

Full description

Saved in:
Bibliographic Details
Published in:Neurobiology of disease 2007-02, Vol.25 (2), p.319-330
Main Authors: Bjørnsen, L.P, Eid, T, Holmseth, S, Danbolt, N.C, Spencer, D.D, de Lanerolle, N.C
Format: Article
Language:English
Subjects:
Adolescent
Adult
Amino Acid Transport System X-AG - metabolism
Astrocytes
Astrocytes - metabolism
Astrocytes - ultrastructure
Child
Child, Preschool
Down-Regulation - physiology
EAAT
Epilepsy - metabolism
Epilepsy - pathology
Epilepsy - physiopathology
Epilepsy, Temporal Lobe - metabolism
Epilepsy, Temporal Lobe - pathology
Epilepsy, Temporal Lobe - physiopathology
Excitatory Amino Acid Transporter 1 - metabolism
Excitatory Amino Acid Transporter 2 - metabolism
Extracellular Fluid - metabolism
Female
GLAST
GLT-1
Glutamate
Glutamic Acid - metabolism
Hippocampus
Hippocampus - metabolism
Hippocampus - pathology
Hippocampus - physiopathology
Humans
Immunohistochemistry
Male
Microscopy, Electron, Transmission
Middle Aged
MTLE
Neurology
Temporal lobe epilepsy
Up-Regulation - physiology
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Abstract Temporal lobe epilepsy (TLE) with hippocampal sclerosis is associated with high extracellular glutamate levels, which could trigger seizures. Down-regulation of glial glutamate transporters GLAST (EAAT1) and GLT-1 (EAAT2) in sclerotic hippocampi may account for such increases. Their distribution was compared immunohistochemically in non-sclerotic and sclerotic hippocampi and localized only in astrocytes, with weaker immunoreactivity for both transporters in areas associated with pronounced neuronal loss, especially in CA1, but no decrease or even an increase in areas with less neuronal loss, like CA2 and the subiculum in the sclerotic group. Such compensatory changes in immunoreactivity may account for the lack of differences between the groups in immunoblot studies as blots show the average concentrations in the samples. These data suggest that differences in glial glutamate transporter distribution between the two groups of hippocampi may be an insufficient explanation for the high levels of extracellular glutamate in sclerotic seizure foci observed through in vivo dialysis studies.
ISSN:0969-9961
1095-953X
DOI:10.1016/j.nbd.2006.09.014