Decreased cortical levels of astrocytic glutamate transport protein GLT-1 in a rat model of posttraumatic epilepsy

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Decreased cortical levels of astrocytic glutamate transport protein GLT-1 in a rat model of posttraumatic epilepsy. / Samuelsson, C; Kumlien, E; Flink, R; Lindholm, D; Ronne-Engström, E.

I: Neuroscience Letters, Vol. 289, Nr. 3, 11.08.2000, s. 185-8.

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Samuelsson, C ; Kumlien, E ; Flink, R ; Lindholm, D ; Ronne-Engström, E. / Decreased cortical levels of astrocytic glutamate transport protein GLT-1 in a rat model of posttraumatic epilepsy. I: Neuroscience Letters. 2000 ; Vol. 289, Nr. 3. s. 185-8.

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TY - JOUR

T1 - Decreased cortical levels of astrocytic glutamate transport protein GLT-1 in a rat model of posttraumatic epilepsy

AU - Samuelsson, C

AU - Kumlien, E

AU - Flink, R

AU - Lindholm, D

AU - Ronne-Engström, E

PY - 2000/8/11

Y1 - 2000/8/11

N2 - The extracellular homeostasis of glutamate in the brain is maintained by the efficient uptake into astroglial cells. The high extracellular glutamate levels seen during seizures are therefore probably a result of both an increased synaptic release and a deranged glutamate uptake. In this study we used immuno-blotting technique to measure the cortical levels of the astrocytic glutamate transport protein (GLT-1) and of the glutamate and aspartate transporting protein (GLAST) in an epilepsy model induced by ferrous chloride injection in the cortex of rats. The levels of GLT-1 were lower in epileptic rats than in controls, day 1 and 5 after induction, but not at 3 months. Glial fibrillary protein (GFAP) levels increased with time in the epileptic model, whereas GLAST and beta-tubulin III remained unchanged compared to controls. The results suggest that the transient decrease of GLT-1 could play a role in epileptogenesis, while recurrent seizure activity may be maintained by other mechanisms.

AB - The extracellular homeostasis of glutamate in the brain is maintained by the efficient uptake into astroglial cells. The high extracellular glutamate levels seen during seizures are therefore probably a result of both an increased synaptic release and a deranged glutamate uptake. In this study we used immuno-blotting technique to measure the cortical levels of the astrocytic glutamate transport protein (GLT-1) and of the glutamate and aspartate transporting protein (GLAST) in an epilepsy model induced by ferrous chloride injection in the cortex of rats. The levels of GLT-1 were lower in epileptic rats than in controls, day 1 and 5 after induction, but not at 3 months. Glial fibrillary protein (GFAP) levels increased with time in the epileptic model, whereas GLAST and beta-tubulin III remained unchanged compared to controls. The results suggest that the transient decrease of GLT-1 could play a role in epileptogenesis, while recurrent seizure activity may be maintained by other mechanisms.

KW - ATP-Binding Cassette Transporters/metabolism

KW - Amino Acid Transport System X-AG

KW - Animals

KW - Astrocytes/drug effects

KW - Cerebral Cortex/metabolism

KW - Disease Models, Animal

KW - Electroencephalography/drug effects

KW - Epilepsy, Post-Traumatic/chemically induced

KW - Ferrous Compounds/adverse effects

KW - Glial Fibrillary Acidic Protein/metabolism

KW - Glutamic Acid/metabolism

KW - Male

KW - Neurons/drug effects

KW - Rats

KW - Rats, Sprague-Dawley

KW - Tubulin/metabolism

U2 - 10.1016/S0304-3940(00)01284-2

DO - 10.1016/S0304-3940(00)01284-2

M3 - Article

C2 - 10961660

VL - 289

SP - 185

EP - 188

JO - Neuroscience Letters

JF - Neuroscience Letters

SN - 0304-3940

IS - 3

ER -