Status epilepticus in well-oxygenated rats causes neuronal necrosis

Nevander, G; Ingvar, M; Auer, R; Siesjö, BK

HERO ID

5383173

Reference Type

Journal Article

Year

1985

Language

English

PMID

4051457

HERO ID 5383173
In Press No
Year 1985
Title Status epilepticus in well-oxygenated rats causes neuronal necrosis
Authors Nevander, G; Ingvar, M; Auer, R; Siesjö, BK
Journal Annals of Neurology
Volume 18
Issue 3
Page Numbers 281-290
Abstract Neuronal necrosis in the brain resulting from status epilepticus of 15 to 120 minutes duration in ventilated and well-oxygenated rats was assessed. Seizures were induced by inhalation of the convulsant gas flurothyl, and terminated by withdrawal of flurothyl and a single injection of thiopental. The animals were allowed to recover for one week, and neuronal damage was assessed by cell counts following subserial sectioning of the brain and microscopical examination of the sections. Infarction of the pars reticulata of the substantia nigra occurred in 5 of the 6 animals with seizure duration of 30 minutes, and in all animals with longer seizure durations. There also was a common affectation of the central parts of the globus pallidus. The pars compacta of the substantia nigra was never affected. After 45 to 120 minutes of seizures, moderate neuronal necrosis was observed in the neocortex (layers 3 and 4), and after 60 to 120 minutes was seen in amygdaloid and thalamic nuclei, as well as in CA4 and CA1 hippocampal pyramidal cells. Notably, CA3 neurons were not damaged nor were dentate granule cells affected. After 120 minutes of seizures, damage regularly affected the neocortex and the ventral-posterior nuclei of the thalamus. A conspicuous feature was the localization of neuronal necrosis at sites close to the ventricles.
Doi 10.1002/ana.410180303
Pmid 4051457
Is Certified Translation No
Dupe Override No
Is Public Yes
Language Text English