Calpain activation is involved in early caspase-independent neurodegeneration in the hippocampus following status epilepticus
(2008) In Journal of Neurochemistry 105(3). p.666-676- Abstract
- 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... (More)
- 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. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1143341
- author
- Araujo, IM ; Gil, Joana LU ; Carreira, BP ; Mohapel, Paul LU ; Petersén, Åsa LU ; Pinheiro, PS ; Soulet, Denis LU ; Bahr, BA ; Brundin, Patrik LU and Carvalho, CM
- organization
- publishing date
- 2008
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Journal of Neurochemistry
- volume
- 105
- issue
- 3
- pages
- 666 - 676
- publisher
- Wiley-Blackwell
- external identifiers
-
- pmid:18088374
- wos:000255139200009
- scopus:42449116702
- pmid:18088374
- ISSN
- 1471-4159
- DOI
- 10.1111/j.1471-4159.2007.05181.x
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Neuronal Survival (013212041), Translational Neuroendocrinology (013210010), Wallenberg Neuroscience Centre, Lund (0131000110)
- id
- 66b86737-7770-4ca0-b07c-225f21973aff (old id 1143341)
- date added to LUP
- 2016-04-01 14:34:40
- date last changed
- 2022-03-29 21:41:14
@article{66b86737-7770-4ca0-b07c-225f21973aff,
abstract = {{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.}},
author = {{Araujo, IM and Gil, Joana and Carreira, BP and Mohapel, Paul and Petersén, Åsa and Pinheiro, PS and Soulet, Denis and Bahr, BA and Brundin, Patrik and Carvalho, CM}},
issn = {{1471-4159}},
language = {{eng}},
number = {{3}},
pages = {{666--676}},
publisher = {{Wiley-Blackwell}},
series = {{Journal of Neurochemistry}},
title = {{Calpain activation is involved in early caspase-independent neurodegeneration in the hippocampus following status epilepticus}},
url = {{http://dx.doi.org/10.1111/j.1471-4159.2007.05181.x}},
doi = {{10.1111/j.1471-4159.2007.05181.x}},
volume = {{105}},
year = {{2008}},
}