Abstract
| Originalsprog | Engelsk |
|---|---|
| Tidsskrift | A P M I S. Acta Pathologica, Microbiologica et Immunologica Scandinavica |
| Vol/bind | 117 |
| Udgave nummer | 4 |
| Sider (fra-til) | 291-301 |
| Antal sider | 10 |
| ISSN | 0903-4641 |
| DOI | |
| Status | Udgivet - 2009 |
Bibliografisk note
Keywords: Adolescent; Adult; Aged; Epilepsy, Temporal Lobe; Excitatory Amino Acid Transporter 1; Excitatory Amino Acid Transporter 2; Female; Glial Fibrillary Acidic Protein; Hippocampus; Humans; Image Processing, Computer-Assisted; Immunohistochemistry; Male; Microscopy, Fluorescence; Middle Aged; Temporal Lobe; Young AdultAdgang til dokumentet
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Excitatory amino acid transporters EAAT-1 and EAAT-2 in temporal lobe and hippocampus in intractable temporal lobe epilepsy. / Sarac, Sinan; Afzal, Shoaib; Broholm, Helle; Madsen, Flemming F; Ploug, Thorkil; Laursen, Henning.
I: A P M I S. Acta Pathologica, Microbiologica et Immunologica Scandinavica, Bind 117, Nr. 4, 2009, s. 291-301.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review
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TY - JOUR
T1 - Excitatory amino acid transporters EAAT-1 and EAAT-2 in temporal lobe and hippocampus in intractable temporal lobe epilepsy
AU - Sarac, Sinan
AU - Afzal, Shoaib
AU - Broholm, Helle
AU - Madsen, Flemming F
AU - Ploug, Thorkil
AU - Laursen, Henning
N1 - Keywords: Adolescent; Adult; Aged; Epilepsy, Temporal Lobe; Excitatory Amino Acid Transporter 1; Excitatory Amino Acid Transporter 2; Female; Glial Fibrillary Acidic Protein; Hippocampus; Humans; Image Processing, Computer-Assisted; Immunohistochemistry; Male; Microscopy, Fluorescence; Middle Aged; Temporal Lobe; Young Adult
PY - 2009
Y1 - 2009
N2 - Intractable temporal lobe epilepsy (TLE) is an invalidating disease and many patients are resistant to medical treatment. Increased glutamate concentration has been found in epileptogenic foci and may induce local over-excitation and cytotoxicity; one of the proposed mechanisms involves reduced extra-cellular clearance of glutamate by excitatory amino acid transporters (EAAT-1 to EAAT-5). EAAT-1 and EAAT-2 are mainly expressed on astroglial cells for the reuptake of glutamate from the extra-cellular space. We have studied the expression of EAAT-1 and EAAT-2 in the hippocampus and temporal lobe in 12 patients with TLE by immunohistochemistry and densitometry. The expression of EAAT-1 and EAAT-2 was reduced to approximately 40% and 25%, respectively, in CA1 of the hippocampus. In the same area, an increased expression of glial fibrillary acid protein (GFAP) at 90% reflected molecular rearrangements and upregulation of GFAP in the existing astrocytes as Ki-67 staining failed to demonstrate any signs of astrocytic proliferation. The aetiology of the reduced expression of EAAT-1 and EAAT-2 remains unclear. The downregulation of EAAT-1 and EAAT-2 may be an adaptive response to neuronal death or it may be a causative event contributing to neuronal death. Further studies of the EAATs and their function are needed to clarify the mechanisms and significance of EAAT-1 and EAAT-2 disappearance in TLE.
AB - Intractable temporal lobe epilepsy (TLE) is an invalidating disease and many patients are resistant to medical treatment. Increased glutamate concentration has been found in epileptogenic foci and may induce local over-excitation and cytotoxicity; one of the proposed mechanisms involves reduced extra-cellular clearance of glutamate by excitatory amino acid transporters (EAAT-1 to EAAT-5). EAAT-1 and EAAT-2 are mainly expressed on astroglial cells for the reuptake of glutamate from the extra-cellular space. We have studied the expression of EAAT-1 and EAAT-2 in the hippocampus and temporal lobe in 12 patients with TLE by immunohistochemistry and densitometry. The expression of EAAT-1 and EAAT-2 was reduced to approximately 40% and 25%, respectively, in CA1 of the hippocampus. In the same area, an increased expression of glial fibrillary acid protein (GFAP) at 90% reflected molecular rearrangements and upregulation of GFAP in the existing astrocytes as Ki-67 staining failed to demonstrate any signs of astrocytic proliferation. The aetiology of the reduced expression of EAAT-1 and EAAT-2 remains unclear. The downregulation of EAAT-1 and EAAT-2 may be an adaptive response to neuronal death or it may be a causative event contributing to neuronal death. Further studies of the EAATs and their function are needed to clarify the mechanisms and significance of EAAT-1 and EAAT-2 disappearance in TLE.
U2 - 10.1111/j.1600-0463.2009.02443.x
DO - 10.1111/j.1600-0463.2009.02443.x
M3 - Journal article
C2 - 19338517
VL - 117
SP - 291
EP - 301
JO - A P M I S. Acta Pathologica, Microbiologica et Immunologica Scandinavica
JF - A P M I S. Acta Pathologica, Microbiologica et Immunologica Scandinavica
SN - 0903-4641
IS - 4
ER -