ALTERED EXPRESSION OF EAAC1 GLUTAMATE TRANSPORTER IN AN EXPERIMENTAL EPILEPSY MODEL

GIRARDI E; AUZMENDI JA; GONZALES NN

Cancún, Mexico

Congreso; 21th biennial meetign; 2007

ISN-ASN

Excesive release of glutamate is envolved in the generation of excitotoxic damage in epilepsy. Glutamate transporter uptake the synaptic released neurotransmitter to prevent accumulation of neurotoxic levels of extracellular glutamate. The sodium dependent transporter EAAC1 is principally enriched in neurons. Adenosine, an endogenous anticonvulsant, inhibits glutamate release from neurons. The objective of this work is to study the effect of the administration of the convulsant 3-mercaptopropionic acid (MP), as an experimental epileptic model, and the adenosine analogue cyclopentyladenosine (CPA) on the EAAC1 glutamate transporter. Methods: Wistar rats (250-300g) were daily injected with MP 45mg/kg i.p. during 4 days, or CPA (2mg/kg) or CPA 30 minutes previous MP (CPA + MP). Control rats were injected with saline. One day after the last injection, brain were processed for immunohystochemical assays using the antibody antiEAAC1and the peroxidase- antiperoxidase technique. Results: In control rats, pyramidal neurons from layer five of the cerebral cortex and in CA1, CA3 hippocampal areas exhibited immunoreactivity and negative immunostaining in astrocytic cells was observed. MP-induced seizure increased EAAC1 expression in both brain areas and an intense immunoreactivity in astrocytes surrounding the vessels was detected. CPA and CPA +Mp increased EAAC1 expression compared with control brain slices. The alteration of the glutamate transporter EAAC1 expression may indicate a compensatory answer or a sign of citotoxic damage.