Status epilepticus triggers caspase-3 activation and necrosis in the immature rat brain

Jerome Niquet; Stéphane Auvin; Mark Archie; Dae Won Seo; Suni Allen; Raman Sankar; Claude G. Wasterlain

doi:10.1111/j.1528-1167.2007.01102.x

Status epilepticus triggers caspase-3 activation and necrosis in the immature rat brain

Jerome Niquet, Stéphane Auvin, Mark Archie, Dae Won Seo, Suni Allen, Raman Sankar, Claude G. Wasterlain

Department of Neurology

Research output: Contribution to journal › Article › peer-review

38 Scopus citations

Abstract

The mode and mechanism of neuronal death induced by status epilepticus (SE) in the immature brain have not been fully characterized. In this study, we analyzed the contribution of neuronal necrosis and caspase-3 activation to CA1 damage following lithium-pilocarpine SE in P14 rat pups. By electron microscopy, many CA1 neurons displayed evidence of early necrosis 6 hours following SE, and the full ultrastructural features of necrosis at 24-72 hours. Caspase-3 was activated in injured (acidophilic) neurons 24 hours following SE, raising the possibility that they died by caspase-dependent "programmed" necrosis.

Original language	English
Pages (from-to)	1203-1206
Number of pages	4
Journal	Epilepsia
Volume	48
Issue number	6
DOIs	https://doi.org/10.1111/j.1528-1167.2007.01102.x
State	Published - Jun 2007

Keywords

Electron microscopy
Hippocampus
Programmed cell death

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10.1111/j.1528-1167.2007.01102.x

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title = "Status epilepticus triggers caspase-3 activation and necrosis in the immature rat brain",

abstract = "The mode and mechanism of neuronal death induced by status epilepticus (SE) in the immature brain have not been fully characterized. In this study, we analyzed the contribution of neuronal necrosis and caspase-3 activation to CA1 damage following lithium-pilocarpine SE in P14 rat pups. By electron microscopy, many CA1 neurons displayed evidence of early necrosis 6 hours following SE, and the full ultrastructural features of necrosis at 24-72 hours. Caspase-3 was activated in injured (acidophilic) neurons 24 hours following SE, raising the possibility that they died by caspase-dependent {"}programmed{"} necrosis.",

keywords = "Electron microscopy, Hippocampus, Programmed cell death",

author = "Jerome Niquet and St{\'e}phane Auvin and Mark Archie and Seo, \{Dae Won\} and Suni Allen and Raman Sankar and Wasterlain, \{Claude G.\}",

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AU - Niquet, Jerome

AU - Auvin, Stéphane

AU - Archie, Mark

AU - Seo, Dae Won

AU - Allen, Suni

AU - Sankar, Raman

AU - Wasterlain, Claude G.

PY - 2007/6

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N2 - The mode and mechanism of neuronal death induced by status epilepticus (SE) in the immature brain have not been fully characterized. In this study, we analyzed the contribution of neuronal necrosis and caspase-3 activation to CA1 damage following lithium-pilocarpine SE in P14 rat pups. By electron microscopy, many CA1 neurons displayed evidence of early necrosis 6 hours following SE, and the full ultrastructural features of necrosis at 24-72 hours. Caspase-3 was activated in injured (acidophilic) neurons 24 hours following SE, raising the possibility that they died by caspase-dependent "programmed" necrosis.

AB - The mode and mechanism of neuronal death induced by status epilepticus (SE) in the immature brain have not been fully characterized. In this study, we analyzed the contribution of neuronal necrosis and caspase-3 activation to CA1 damage following lithium-pilocarpine SE in P14 rat pups. By electron microscopy, many CA1 neurons displayed evidence of early necrosis 6 hours following SE, and the full ultrastructural features of necrosis at 24-72 hours. Caspase-3 was activated in injured (acidophilic) neurons 24 hours following SE, raising the possibility that they died by caspase-dependent "programmed" necrosis.

KW - Electron microscopy

KW - Hippocampus

KW - Programmed cell death

UR - https://www.scopus.com/pages/publications/34249805412

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AN - SCOPUS:34249805412

SN - 0013-9580

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SP - 1203

EP - 1206

JO - Epilepsia

JF - Epilepsia

IS - 6

ER -

Status epilepticus triggers caspase-3 activation and necrosis in the immature rat brain

Abstract

Keywords

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