Donate Help Contact The AHA Sign In Home
American Heart Association
Stroke
Search: search_blue_button Advanced Search
Stroke. 1998;29:1967-1971

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Colbourne, F.
Right arrow Articles by Dietrich, W. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Colbourne, F.
Right arrow Articles by Dietrich, W. D.

(Stroke. 1998;29:1967-1971.)
© 1998 American Heart Association, Inc.


Original Contributions

Behavioral Testing Does Not Exacerbate Ischemic CA1 Damage in Gerbils

Frederick Colbourne, PhD; Roland N. Auer, MD, PhD; Garnette R. Sutherland, MD

From the Departments of Pathology (F.C., R.N.A.) and Clinical Neurosciences (Division of Neurosurgery) (G.R.S.), Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada.

Correspondence to Frederick Colbourne, PhD, Department of Pathology, Faculty of Medicine, University of Calgary, 3330 Hospital Dr NW, Calgary, Alberta, Canada T2N 4N1. E-mail colbourn{at}acs.ucalgary.ca

Background and Purpose—Previous research studying ablative lesions has suggested that functional use may exacerbate brain injury. If true, this would have considerable ramifications not only for the mechanistic understanding of neuronal injury but also for the clinical use of physiotherapy. In this report the hypothesis that behavioral use of brain tissue exacerbates ischemic hippocampal injury was tested.

Methods—Gerbils were subjected to sham operation or 5 minutes of normothermic ischemia. To produce borderline hippocampal CA1 injury and enhance susceptibility to exacerbation, 2 of 3 ischemic groups were cooled (>48 hours) beginning at 6 hours after ischemia. Increased use of the hippocampus was produced by a battery of tests involving 3 novel small mazes, a T maze, and an open field. One hypothermic group was not tested and served as a control.

Results—Behavioral testing failed to worsen ischemic damage since neuronal loss in the behaviorally tested and untested hypothermic groups was 12% and 8%, respectively, while that in the untreated ischemic group was 81% at a 1-month survival. Accordingly, protected CA1 cells tolerated the neuronal activity associated with behavioral testing. Concomitant with marked CA1 neuroprotection, a significant reduction in behavioral deficits with the hypothermic treatment was observed. Importantly, behavioral testing was found to transiently elevate brain temperature.

Conclusions—CA1 neuronal survival was unaffected by behavioral testing or the associated mild fever. Hypothermia delayed for 6 hours provided sustainable CA1 neuroprotection.

Editorial Comment

W. Dalton Dietrich, PhD, Guest Editor

Departments of Neurological Surgery and Neurology, University of Miami School of Medicine, Miami, Florida




This article has been cited by other articles:


Home page
StrokeHome page
H. Dong, F. Moody-Corbett, F. Colbourne, Q. Pittman, and D. Corbett
Electrophysiological Properties of CA1 Neurons Protected by Postischemic Hypothermia in Gerbils
Stroke, March 1, 2001; 32(3): 788 - 795.
[Abstract] [Full Text] [PDF]


Home page
StrokeHome page
S. T. Bland, T. Schallert, R. Strong, J. Aronowski, J. C. Grotta, and D. M. Feeney
Early Exclusive Use of the Affected Forelimb After Moderate Transient Focal Ischemia in Rats : Functional and Anatomic Outcome Editorial Comment: Functional and Anatomic Outcome
Stroke, May 1, 2000; 31(5): 1144 - 1152.
[Abstract] [Full Text] [PDF]