Abstract：
: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.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Samuelsson C,Kumlien E,Flink R,Lindholm D,Ronne-Engström Edoi
10.1016/s0304-3940(00)01284-2keywords:
subject
Has Abstractpub_date
2000-08-11 00:00:00pages
185-8issue
3eissn
0304-3940issn
1872-7972pii
S0304394000012842journal_volume
289pub_type
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