title: Fundamental interstrain differences in cortical activity between Wistar and Sprague-Dawley rats during global ischemia.
abstract: Four-vessel occlusion (4VO), a frequently used model of global cerebral ischemia in rats, results in a dysfunction in wide brain areas, including the cerebral cortex and hippocampus. However, there are pronounced differences in response to global ischemia between the laboratory rat strains used in these studies. In the present work, the immediate acute effects of 4VO-induced global ischemia on the spontaneous electrocorticogram (ECoG) signals were analyzed in Wistar and Sprague-Dawley rats. The ECoG was isoelectric during the 10 min of global cerebral ischemia in Wistar rats and the first burst (FB) was seen 10-13 min after the start of reperfusion. In Sprague-Dawley rats, the FB was detected immediately after the start of 4VO or a few seconds later. The burst suppression ratio (BSR) in Wistar rats decreased to 45% in 5 min after FB, and after 25 min it was approximately 40%. In Sprague-Dawley rats, the BSR was 55% immediately after the FB and it decreased steeply to reach 0% by 10 min. There was also a significant difference between the two strains in the frequency composition of the ECoG pattern. The power spectral densities of the two strains differed virtually throughout the post-ischemic state. The histological results (Evans Blue, Cresyl Violet and Fluoro Jade C stainings) supplemented the electrophysiological data: the neuronal damage in the CA1 pyramids in Wistar rats was severe, whereas in the Sprague-Dawley animals it was only partial. These observations clearly demonstrate that the use of different rat strains (e.g. Wistar vs. Sprague-Dawley) can be a source of considerable variability in the results of acute experiments on global ischemia and it is important that the laboratory rats used in such experiments should be carefully chosen.
authors.affiliation: University of Szeged, Department of Physiology, Anatomy and Neuroscience, Közép fasor 52, H-6726 Szeged, Hungary.
authors.forename: J
authors.initials: J
authors.lastname: Fuzik
authors.forename: L
authors.initials: L
authors.lastname: Gellért
authors.forename: G
authors.initials: G
authors.lastname: Oláh
authors.forename: J
authors.initials: J
authors.lastname: Herédi
authors.forename: K
authors.initials: K
authors.lastname: Kocsis
authors.forename: L
authors.initials: L
authors.lastname: Knapp
authors.forename: D
authors.initials: D
authors.lastname: Nagy
authors.forename: Z T
authors.initials: ZT
authors.lastname: Kincses
authors.forename: Z
authors.initials: Z
authors.lastname: Kis
authors.forename: T
authors.initials: T
authors.lastname: Farkas
authors.forename: J
authors.initials: J
authors.lastname: Toldi
mesh_terms: D000818:Animals; D002545:Brain Ischemia / Q000235:genetics* / Q000503:physiopathology*; D002540:Cerebral Cortex / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017208:Rats, Wistar; D013045:Species Specificity