Pilocarpine-induced status epilepticus increases glutamate release in rat hippocampal synaptosomes.
A pronounced glutamate release has been related to neuronal death in several structures due to status epilepticus (SE). We investigated the glutamate uptake and release by both cortical and hippocampal synaptosome in pilocarpine model of epilepsy. Animals were submitted to long-lasting SE (12 h) induced by pilocarpine and compared with non-treated animals. Animals presenting SE did not modify the glutamate uptake by synaptosomes. An increase in the glutamate efflux in the absence (1.43-fold) and in the presence of KCl (1.25-fold) was found in hippocampal synaptosomes. Pilocarpine added to the medium did not modify the glutamate release profile, showing that SE is necessary to modify the glutamate release. As the glutamate uptake is not modified, the hippocampal excitotoxicity may be related to impairment only in the mechanism of the glutamate release.
Costa
Maricilia S
MS
Disciplina de Neurologia Experimental, UNIFESP-EPM, São Paulo, Brazil. mscosta@univap.br
Rocha
João B T
JB
Perosa
Sandra R
SR
Cavalheiro
Esper A
EA
Naffah-Mazzacoratti
Maria da Graça
Mda G
D000818:Animals; D018698:Glutamic Acid / Q000378:metabolism*; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D010862:Pilocarpine / Q000633:toxicity*; D051381:Rats; D017208:Rats, Wistar; D013226:Status Epilepticus / Q000139:chemically induced / Q000378:metabolism*; D013574:Synaptosomes / Q000187:drug effects / Q000378:metabolism*
D010862:Pilocarpine; D018698:Glutamic Acid