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Effect of inherent epileptic seizures on brain injury after transient cerebral ischemia in Mongolian gerbils

Herrmann, Martina ; Stern, Martin ; Vollenweider, Florence ; Nitsch, Cordula

In: Experimental Brain Research, 2004, vol. 154, no. 2, p. 176-182

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    Titel
    • Effect of inherent epileptic seizures on brain injury after transient cerebral ischemia in Mongolian gerbils
    Autor
    • Herrmann, Martina. Section of Neuroanatomy, Institute of Anatomy, University of Basel, Pestalozzistr. 20, 4056 Basel, Switzerland
    • Stern, Martin. Section of Neuroanatomy, Institute of Anatomy, University of Basel, Pestalozzistr. 20, 4056 Basel, Switzerland
    • Vollenweider, Florence. Section of Neuroanatomy, Institute of Anatomy, University of Basel, Pestalozzistr. 20, 4056 Basel, Switzerland
    • Nitsch, Cordula. Section of Neuroanatomy, Institute of Anatomy, University of Basel, Pestalozzistr. 20, 4056 Basel, Switzerland
    Dokumententyp
    • Postprint
    Sprache
    • Englisch
    Veröffentlicht in
    • Experimental Brain Research, 2004, vol. 154, no. 2, p. 176-182. Springer-Verlag; http://www.springer.de
    Andere elektronische Ausgabe
    OAI-PMH-ID
    • oai:doc.rero.ch:312574
    Summary
    Subthreshold excitotoxic stimuli such as brief cerebral ischemia or chemically induced seizures modulate brain injury resulting from subsequent transient ischemia. Depending on the delay between the two insults, either tolerance or cumulative damage will develop. We were interested whether non-chemically induced inherent epileptic seizures as they occur in Mongolian gerbils have an effect on the outcome of a transient global ischemia, i.e., whether they are an interfering variable in ischemia experiments. Occurrence of spontaneous seizures in adult male gerbils was registered with a video-controlled seizure monitoring system. Bilateral occlusion of common carotid arteries was carried out 2h or 24h after the last generalized seizure. After 4days survival, the extent of ischemia-induced neuronal damage and glial activation were assessed in the hippocampus and striatum. No significant difference in the ischemia induced nerve cell loss was observed in cresyl violet stained sections between the 2-h or 24-h interval gerbils. Neuronal expression of endothelial nitric oxide synthase in CA1 disappeared with neuronal degeneration. Distribution and degree of upregulation of glial fibrillary acidic protein as marker for astrocytes did not differ between the two groups. We concluded that non-chemically induced inherent epileptic seizures neither protect the gerbil brain from injury nor augment the degree of damage resulting from transient forebrain ischemia. Thus, inherent epileptic seizures do not influence the outcome of the insult, making the gerbil a reliable model for studies on transient brain ischemia