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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Reduced hippocampal manganese-enhanced MRI (MEMRI) signal during pilocarpine-induced status epilepticus: Edema or apoptosis?

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Author(s):
Malheiros, Jackeline Moraes [1] ; Persike, Daniele Suzete [2] ; Cardoso de Castro, Leticia Urbana [3] ; Cunha Sanches, Talita Rojas [3] ; Andrade, Lucia da Conceicao [3] ; Tannus, Alberto [4] ; Covolan, Luciene [1]
Total Authors: 7
Affiliation:
[1] Univ Fed Sao Paulo, UNIFESP, Dept Fisiol, BR-0402306 Sao Paulo - Brazil
[2] Univ Fed Sao Paulo, UNIFESP, Dept Neurol & Neurocirurgia, BR-0402306 Sao Paulo - Brazil
[3] Univ Sao Paulo, Fac Med, Dept Nefrol, Sao Paulo - Brazil
[4] Univ Sao Paulo, IFSC, Ctr Imagens & Espectroscopia Vivo Ressonancia Mag, BR-13566590 Sao Carlos, SP - Brazil
Total Affiliations: 4
Document type: Journal article
Source: Epilepsy Research; v. 108, n. 4, p. 644-652, MAY 2014.
Web of Science Citations: 11
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. (AU)

FAPESP's process: 05/56663-1 - Magnetic resonance imaging and in vivo spectroscopy center for animal model studies
Grantee:Alberto Tannús
Support Opportunities: Inter-institutional Cooperation in Support of Brain Research (CINAPCE) - Thematic Grants