Hyperoxia is not an essential condition for status epilepticus induced cell death in organotypic hippocampal slice cultures.
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 1h 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.
Pomper
Jörn K
JK
Johannes Müller Institute of Physiology, University Hospital Charité, Humboldt University Berlin, Tucholskystrasse 2, D-10117 Berlin, Germany. joern.pomper@gmx.de
Hoffmann
Ulrike
U
Kovács
Richard
R
Gabriel
Siegrun
S
Heinemann
Uwe
U
D000818:Animals; D016923:Cell Death / Q000187:drug effects / Q000502:physiology; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism*; D018496:Hyperoxia / Q000378:metabolism* / Q000473:pathology*; D008274:Magnesium / Q000008:administration & dosage; D009924:Organ Culture Techniques; D051381:Rats; D017208:Rats, Wistar; D013226:Status Epilepticus / Q000378:metabolism* / Q000473:pathology*
D008274:Magnesium