Hyperoxia is not an essential condition for status epilepticus induced cell death in organotypic hippocampal slice cultures

Jörn K. Pomper; Ulrike Hoffmann; Richard Kovács; Siegrun Gabriel; Uwe Heinemann

doi:10.1016/j.eplepsyres.2004.03.002

Hyperoxia is not an essential condition for status epilepticus induced cell death in organotypic hippocampal slice cultures

Jörn K. Pomper, Ulrike Hoffmann, Richard Kovács, Siegrun Gabriel, Uwe Heinemann

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

10 Scopus citations

Abstract

The low Mg²⁺ model of epilepsy in organotypic hippocampal slice cultures is used to elucidate the mechanism underlying neuronal cell death following sustained epileptiform activity. However, the high oxygen tension of 95% widely used in this model is capable of inducing neuronal cell death by itself. Here we demonstrate that even under normoxic conditions 1 h of epileptiform activity induced neuronal cell death as assessed by Propidium Iodide uptake. We conclude that hyperoxia is not essential for status epilepticus induced neuronal cell death in this model.

Original language	English (US)
Pages (from-to)	61-65
Number of pages	5
Journal	Epilepsy Research
Volume	59
Issue number	1
DOIs	https://doi.org/10.1016/j.eplepsyres.2004.03.002
State	Published - Mar 2004
Externally published	Yes

Keywords

Cell death
High oxygen
Propidum Iodide
ROS
Seizure
Spreading depression

ASJC Scopus subject areas

Neurology
Clinical Neurology

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10.1016/j.eplepsyres.2004.03.002

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title = "Hyperoxia is not an essential condition for status epilepticus induced cell death in organotypic hippocampal slice cultures",

abstract = "The low Mg2+ model of epilepsy in organotypic hippocampal slice cultures is used to elucidate the mechanism underlying neuronal cell death following sustained epileptiform activity. However, the high oxygen tension of 95% widely used in this model is capable of inducing neuronal cell death by itself. Here we demonstrate that even under normoxic conditions 1 h of epileptiform activity induced neuronal cell death as assessed by Propidium Iodide uptake. We conclude that hyperoxia is not essential for status epilepticus induced neuronal cell death in this model.",

keywords = "Cell death, High oxygen, Propidum Iodide, ROS, Seizure, Spreading depression",

author = "Pomper, {J{\"o}rn K.} and Ulrike Hoffmann and Richard Kov{\'a}cs and Siegrun Gabriel and Uwe Heinemann",

note = "Funding Information: We are grateful for technical assistance in data evaluation and imaging analysis to Dr. Herbert Siegmund and Dr. Hans-J{\"u}rgen Gabriel as well as to Sieglinde Latta for assistance in culture work. This study was supported by the graduate college “Damage mechanisms in the central nervous system—studies with imaging methods” and the SFB 507, TP C4 as well as by a BMBF grant contract no. 0310974.",

year = "2004",

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doi = "10.1016/j.eplepsyres.2004.03.002",

language = "English (US)",

volume = "59",

pages = "61--65",

journal = "Epilepsy Research",

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publisher = "Elsevier",

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T1 - Hyperoxia is not an essential condition for status epilepticus induced cell death in organotypic hippocampal slice cultures

AU - Pomper, Jörn K.

AU - Hoffmann, Ulrike

AU - Kovács, Richard

AU - Gabriel, Siegrun

AU - Heinemann, Uwe

N1 - Funding Information: We are grateful for technical assistance in data evaluation and imaging analysis to Dr. Herbert Siegmund and Dr. Hans-Jürgen Gabriel as well as to Sieglinde Latta for assistance in culture work. This study was supported by the graduate college “Damage mechanisms in the central nervous system—studies with imaging methods” and the SFB 507, TP C4 as well as by a BMBF grant contract no. 0310974.

PY - 2004/3

Y1 - 2004/3

N2 - The low Mg2+ model of epilepsy in organotypic hippocampal slice cultures is used to elucidate the mechanism underlying neuronal cell death following sustained epileptiform activity. However, the high oxygen tension of 95% widely used in this model is capable of inducing neuronal cell death by itself. Here we demonstrate that even under normoxic conditions 1 h of epileptiform activity induced neuronal cell death as assessed by Propidium Iodide uptake. We conclude that hyperoxia is not essential for status epilepticus induced neuronal cell death in this model.

AB - The low Mg2+ model of epilepsy in organotypic hippocampal slice cultures is used to elucidate the mechanism underlying neuronal cell death following sustained epileptiform activity. However, the high oxygen tension of 95% widely used in this model is capable of inducing neuronal cell death by itself. Here we demonstrate that even under normoxic conditions 1 h of epileptiform activity induced neuronal cell death as assessed by Propidium Iodide uptake. We conclude that hyperoxia is not essential for status epilepticus induced neuronal cell death in this model.

KW - Cell death

KW - High oxygen

KW - Propidum Iodide

KW - ROS

KW - Seizure

KW - Spreading depression

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DO - 10.1016/j.eplepsyres.2004.03.002

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AN - SCOPUS:2342568854

SN - 0920-1211

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JO - Epilepsy Research

JF - Epilepsy Research

IS - 1

ER -

Hyperoxia is not an essential condition for status epilepticus induced cell death in organotypic hippocampal slice cultures

Abstract

Keywords

ASJC Scopus subject areas

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