GLT-1 expression and Glu uptake in rat cerebral cortex are increased by phencyclidine.
Giorgia Fattorini, Marcello Melone, Luca Bragina, Chiara Candiracci, Andrea Cozzi, Domenico E Pellegrini-Giampietro, Monica Torres-Ramos, Alberto Pérez-Samartín, Carlos Matute, Fiorenzo Conti
Glia September 2008 DOI: 10.1002/glia.20700 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Experimental animal study Peer reviewed |
|---|---|
| Population | Rats (frontal cortex, brain slices, and neuron/astrocyte co-cultures) |
| Intervention | Phencyclidine (PCP) |
| Dose | 10 mg/kg/day |
| Duration | 7 days |
| Key findings | PCP administered at 10 mg/kg/day for 7 days increased GLT-1/EAAT2 expression and sodium-dependent glutamate uptake while reducing basal extracellular glutamate, without inducing toxicity under these conditions. The authors propose that PCP elevates cortical GLT-1, thereby enhancing glutamate clearance and lowering extracellular glutamate. |
Abstract
Using western blottings, microdialysis, and functional assays we tested the hypothesis that phencyclidine (PCP) modifies the expression and function of glutamate (Glu) transporters in the rat frontal cortex. Western blotting studies revealed that administration of PCP (10 mg/kg/day; 7 days) increased significantly the expression of the astrocytic Glu transporter GLT-1/EAAT2. Functional studies showed that PCP increased significantly Na+-dependent Glu uptake in slices and in neuron/astrocyte co-cultures, and microdialysis studies evidenced that PCP treatment reduced basal Glu output. In our experimental conditions, PCP did not induce toxicity. These studies show that PCP increases the expression of GLT-1 in the cerebral cortex, thereby increasing Glu uptake and reducing extracellular [Glu].
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