Pilocarpine-induced status epilepticus increases glutamate release in rat hippocampal synaptosomes
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作者:
Costa, MS
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Univ Fed Sao Paulo, Disciplina Neurol Expt, EPM, Sao Paulo, BrazilUNIVAP, Inst Pesquisa & Desenvolvimento, BR-12244000 Sao Jose Dos Campos, SP, Brazil
Costa, MS
[2
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Rocha, JBT
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机构:UNIVAP, Inst Pesquisa & Desenvolvimento, BR-12244000 Sao Jose Dos Campos, SP, Brazil
Rocha, JBT
Perosa, SR
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机构:UNIVAP, Inst Pesquisa & Desenvolvimento, BR-12244000 Sao Jose Dos Campos, SP, Brazil
Perosa, SR
Cavalheiro, EA
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机构:UNIVAP, Inst Pesquisa & Desenvolvimento, BR-12244000 Sao Jose Dos Campos, SP, Brazil
Cavalheiro, EA
Naffah-Mazzacoratti, MDG
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机构:UNIVAP, Inst Pesquisa & Desenvolvimento, BR-12244000 Sao Jose Dos Campos, SP, Brazil
Naffah-Mazzacoratti, MDG
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[1] UNIVAP, Inst Pesquisa & Desenvolvimento, BR-12244000 Sao Jose Dos Campos, SP, Brazil
[2] Univ Fed Sao Paulo, Disciplina Neurol Expt, EPM, Sao Paulo, Brazil
[3] Univ Fed Santa Maria, Ctr Ciencias Nat & Exatas, Dept Quim, Santa Maria, RS, Brazil
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. (C) 2003 Elsevier Ireland Ltd. All rights reserved.