Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/37730
Title: Reduced hippocampal manganese-enhanced MRI (MEMRI) signal during pilocarpine-induced status epilepticus: Edema or apoptosis?
Authors: Malheiros, Jackeline Moraes [UNIFESP]
Persike, Daniele Suzete [UNIFESP]
Cardoso de Castro, Leticia Urbana
Cunha Sanches, Talita Rojas
Andrade, Lucia da Conceicao
Tannus, Alberto
Covolan, Luciene [UNIFESP]
Universidade Federal de São Paulo (UNIFESP)
Universidade de São Paulo (USP)
Keywords: Pilocarpine
Epilepsy
Manganese-enhanced magnetic resonance imaging
Edema
Apoptosis
Hippocampus
Issue Date: 1-May-2014
Publisher: Elsevier B.V.
Citation: Epilepsy Research. Amsterdam: Elsevier B.V., v. 108, n. 4, p. 644-652, 2014.
Abstract: Manganese-enhanced MRI (MEMRI) has been considered a surrogate marker of Ca+2 influx into activated cells and tracer of neuronal active circuits. However, the induction of status epilepticus (SE) by kainic acid does not result in hippocampal MEMRI hypersignal, in spite of its high cell activity. Similarly, short durations of status (5 or 15 min) induced by pilocarpine did not alter the hippocampal MEMRI, while 30 min of SE even reduced MEMRI signal Thus, this study was designed to investigate possible explanations for the absence or decrease of MEMRI signal after short periods of SE. We analyzed hippocampal caspase-3 activation (to evaluate apoptosis), T-2 relaxometry (tissue water content) and aquaporin 4 expression (water-channel protein) of rats subjected to short periods of pilocarpine-induced SE. for the time periods studied here, apoptotic cell death did not contribute to the decrease of the hippocampal MEMRI signal. However, T-2 relaxation was higher in the group of animals subjected to 30 min of SE than in the other SE or control groups. This result is consistent with higher AQP-4 expression during the same time period. Based on apoptosis and tissue water content analysis, the low hippocampal MEMRI signal 30 min after SE can potentially be attributed to local edema rather than to cell death. (C) 2014 Elsevier B.V. All rights reserved.
URI: http://repositorio.unifesp.br/handle/11600/37730
ISSN: 0920-1211
Other Identifiers: http://dx.doi.org/10.1016/j.eplepsyres.2014.02.007
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