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

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Affiliations

  • 1. Departamento de Fisiologia, Universidade Federal de São Paulo-UNIFESP, São Paulo 04023-06, SP, Brazil; Centro de Imagens e Espectroscopia in vivo por Ressonância Magnética (CIERMag), Instituto de Física de São Carlos, Universidade de São Paulo (IFSC-USP), São Carlos 13566-590, SP, Brazil.
      Authors
    • Malheiros JM 1
    (1 author)
  • 2. Departamento de Neurologia e Neurocirurgia, Universidade Federal de São Paulo-UNIFESP, São Paulo, SP, Brazil.
      Authors
    • Persike DS 2
    (1 author)
  • 3. Departamento de Nefrologia, Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP, Brazil.
      Authors
    • Castro LU 3
    • Sanches TR 3
    • Andrade Lda C 3
    (3 authors)
  • 4. Centro de Imagens e Espectroscopia in vivo por Ressonância Magnética (CIERMag), Instituto de Física de São Carlos, Universidade de São Paulo (IFSC-USP), São Carlos 13566-590, SP, Brazil.
      Authors
    • Tannús A 4
    (1 author)
  • 5. Departamento de Fisiologia, Universidade Federal de São Paulo-UNIFESP, São Paulo 04023-06, SP, Brazil.
      Authors
    • Covolan L 5
    (1 author)

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Epilepsy Research, 19 Feb 2014, 108(4):644-652
https://doi.org/10.1016/j.eplepsyres.2014.02.007 PMID: 24630048 

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 15min) 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), 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 30min 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 30min after SE can potentially be attributed to local edema rather than to cell death.

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Read article at publisher's site: https://doi.org/10.1016/j.eplepsyres.2014.02.007

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