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Calpain activation is involved in early caspase-independent neurodegeneration in the hippocampus following status epilepticus

In English

Författare

  • IM Araujo
  • Joana Gil
  • BP Carreira
  • Paul Mohapel
  • Åsa Petersén
  • PS Pinheiro
  • Denis Soulet
  • BA Bahr
  • Patrik Brundin
  • CM Carvalho

Summary, in English

Evidence for increased calpain activity has been described in the hippocampus of rodent models of temporal lobe epilepsy. However, it is not known whether calpains are involved in the cell death that accompanies seizures. In this work, we characterized calpain activation by examining the proteolysis of calpain substrates and in parallel we followed cell death in the hippocampus of epileptic rats. Male Wistar rats were injected with kainic acid (KA; 10 mg/kg) intraperitoneally and sacrificed 24h later, after development of grade 5 seizures. We observed a strong Fluoro-Jade labelling in the CA1 and CA3 areas of the hippocampus in the rats that received KA, as compared to saline-treated rats. Immunohistochemistry and Western blot analysis for the calpain-derived breakdown products of spectrin (SBDP) showed evidence of increased calpain activity in the same regions of the hippocampus where cell death is observed. No evidence was found for caspase activation, in the same conditions. Treatment with the calpain inhibitor MDL 28170 significantly prevented the neurodegeneration observed in CA1. Taken together, our data suggest that early calpain activation, but not caspase activation, is involved in neurotoxicity in the hippocampus after status epilepticus.

Publiceringsår

2008

Språk

Engelska

Sidor

666-676

Publikation/Tidskrift/Serie

Journal of Neurochemistry

Volym

105

Issue

3

Dokumenttyp

Artikel i tidskrift

Förlag

Wiley-Blackwell

Ämne

  • Neurosciences

Status

Published

Forskningsgrupp

  • Translational Neuroendocrinology

ISBN/ISSN/Övrigt

  • ISSN: 1471-4159