Article ID Journal Published Year Pages File Type
10958185 Neurochemistry International 2013 9 Pages PDF
Abstract
The majority of glutamate released during neurotransmission is uptaken into astrocytes through the glial glutamate transporter GLT-1, by which extracellular glutamate is inactivated. In this study, we determined whether GLT-1 mediated the astrocyte regulation of the cell fate of neural stem/progenitor cells (NSCs) by glutamate reuptake. The astrocytes stimulated neuronal lineage selection but inhibited glial lineage cells. However, all these effects were reversed after siRNA-targeting GLT-1 was delivered into astrocytes by lentiviral vectors. NSC and astrocyte co-culture also increased the synaptophysin protein levels of NSC-derived new neurons through GLT-1. Glutamate was found to be present in the supernatants of the co-culture and astrocytes under different medium conditions, which may be attributed to the slower rate of clearance of the released glutamate. Dysfunctional glutamate reuptake may be the major consequence of GLT-1 functional silence in astrocytes. These results indicated that astrocytes regulated NSCs in reactive astrogliosis, neuronal generation, and synaptic function through GLT-1.
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