NDLI: Reversed Actrocytic GLT-1 during Ischemia is Crucial to Excitotoxic Death of Neurons, but Contributes to the Survival of Astrocytes themselves

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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

Content Provider	Springer Nature Link
Author	Kosugi, Tatsuro Kawahara, Koichi
Copyright Year	2006
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$^{+}$/Ca$^{2+}$-exchanger (NCX). The reversed NCX then caused Ca$^{2+}$ 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.
Starting Page	933
Ending Page	943
Page Count	11
File Format	PDF
ISSN	03643190
Journal	Neurochemical Research
Volume Number	31
Issue Number	7
e-ISSN	15736903
Language	English
Publisher	Kluwer Academic Publishers-Plenum Publishers
Publisher Date	2006-07-08
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Ischemia Reversed GLT-1 Astrocyte damage Na$^{+}$/Ca$^{2+}$ exchanger Excitotoxic neuronal death Biochemistry Neurology Neurosciences
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry Cellular and Molecular Neuroscience

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