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Reversed actrocytic GLT-1 during ischemia is crucial to excitotoxic death of neurons, but contributes to the survival of astrocytes themselves.
Title: | Reversed actrocytic GLT-1 during ischemia is crucial to excitotoxic death of neurons, but contributes to the survival of astrocytes themselves. |
Authors: | Kosugi, Tatsuro Browse this author | Kawahara, Koichi Browse this author →KAKEN DB |
Keywords: | Ischemia | Reversed GLT-1 | Astrocyte damage | Na+/Ca2+ exchanger | Excitotoxic neuronal death |
Issue Date: | Jul-2006 |
Publisher: | Springer Netherlands |
Journal Title: | Neurochemical Research |
Volume: | 31 |
Issue: | 7 |
Start Page: | 933 |
End Page: | 943 |
Publisher DOI: | 10.1007/s11064-006-9099-6 |
PMID: | 16830212 |
Abstract: | During ischemia, the operation of astrocytic/neuronal glutamate transporters is reversed and glutamate and Na+ are co-transported to the extracellular space. This study aims to investigate whether this reversed operation of glutamate transporters has any functional meanings for astrocytes themselves. Oxygen/glucose deprivation (OGD) of neuron/astrocyte co-cultures resulted in the massive death of neurons, and the cell death was significantly reduced by treatment with either AP5 or DHK. In cultured astrocytes with little GLT-1 expression, OGD produced Na+ overload, resulting in the reversal of astrocytic Na+/Ca2+-exchanger (NCX). The reversed NCX then caused Ca2+ overload leading to the damage of astrocytes. In contrast, the OGD-induced Na+ overload and astrocytic damage were significantly attenuated in PACAP-treated astrocytes with increased GLT-1 expression, and the attenuation was antagonized by treatment with DHK. These results suggested that the OGD-induced reversal of GLT-1 contributed to the survival of astrocytes themselves by releasing Na+ with glutamate via reversed GLT-1. |
Rights: | The original publication is available at www.springerlink.com |
Type: | article (author version) |
URI: | http://hdl.handle.net/2115/14610 |
Appears in Collections: | 情報科学院・情報科学研究院 (Graduate School of Information Science and Technology / Faculty of Information Science and Technology) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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Submitter: 河原 剛一
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