title: Effect of inherent epileptic seizures on brain injury after transient cerebral ischemia in Mongolian gerbils.
abstract: 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 2 h or 24 h after the last generalized seizure. After 4 days 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.
authors.affiliation: Section of Neuroanatomy, Institute of Anatomy, University of Basel, Pestalozzistr. 20, 4056 Basel, Switzerland.
authors.forename: Martina
authors.initials: M
authors.lastname: Herrmann
authors.forename: Martin
authors.initials: M
authors.lastname: Stern
authors.forename: Florence
authors.initials: F
authors.lastname: Vollenweider
authors.forename: Cordula
authors.initials: C
authors.lastname: Nitsch
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000166:cytology / Q000378:metabolism; D002544:Cerebral Infarction / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D003342:Corpus Striatum / Q000473:pathology / Q000503:physiopathology*; D004195:Disease Models, Animal; D004827:Epilepsy / Q000150:complications / Q000151:congenital / Q000503:physiopathology*; D005849:Gerbillinae; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005911:Gliosis / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D006624:Hippocampus / Q000473:pathology / Q000503:physiopathology*; D002546:Ischemic Attack, Transient / Q000150:complications / Q000503:physiopathology*; D008297:Male; D009410:Nerve Degeneration / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III; D011930:Reaction Time / Q000502:physiology
chemical_list: D005904:Glial Fibrillary Acidic Protein; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III