Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6015567 | Epilepsy Research | 2014 | 9 Pages |
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 15Â min) induced by pilocarpine did not alter the hippocampal MEMRI, while 30Â 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), T2 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, T2 relaxation was higher in the group of animals subjected to 30Â 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 30Â min after SE can potentially be attributed to local edema rather than to cell death.
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Authors
Jackeline Moraes Malheiros, Daniele Suzete Persike, Leticia Urbano Cardoso de Castro, Talita Rojas Cunha Sanches, Lúcia da Conceição Andrade, Alberto Tannús, Luciene Covolan,