Donate Help Contact The AHA Sign In Home
American Heart Association
Stroke
Search: search_blue_button Advanced Search
This Article
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 arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Volpe, B. T.
Right arrow Articles by Davis, H. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Volpe, B. T.
Right arrow Articles by Davis, H. P.

Stroke, Vol 15, 558-562, Copyright © 1984 by American Heart Association


ARTICLES

Behavioral performance of rats following transient forebrain ischemia

BT Volpe, WA Pulsinelli, J Tribuna and HP Davis

Rats subjected to transient forebrain ischemic injury by the method of four vessel occlusion (4-VO) develop irreversible injury to select populations of vulnerable neurons which include pyramidal cells in the CA-1 region of the hippocampus. This brain area is thought to be crucial for learning and memory. Rats subjected to 30 minutes of 4-VO, and then cerebral reperfusion were tested on a radial 8-arm maze task after they had recovered. The data shows that both 4-VO and control animals improve their performance over trials, but that 4-VO rats are impaired on "working" and "reference" tasks. The data suggest that 4-VO rats' impaired "working" performance is permanent, compared to their transient "reference" impairment. Alterations in sensorimotor activity could not account for these performance deficits since control and 4-VO rats demonstrated equivalent choice time per maze arm. Performance deficits in rats following forebrain ischemic injury may be similar to some of the cognitive deficits found in humans survivors of cerebral hypoxia-ischemia.


This article has been cited by other articles:


Home page
NeuroscientistHome page
J. Epsztein, Y. Ben-Ari, A. Represa, and V. Crepel
Late-Onset Epileptogenesis and Seizure Genesis: Lessons From Models of Cerebral Ischemia
Neuroscientist, February 1, 2008; 14(1): 78 - 90.
[Abstract] [PDF]


Home page
J. Appl. Physiol.Home page
G. S. Mitchell and S. M. Johnson
Plasticity in Respiratory Motor Control: Invited Review: Neuroplasticity in respiratory motor control
J Appl Physiol, January 1, 2003; 94(1): 358 - 374.
[Abstract] [Full Text] [PDF]


Home page
J. Neurosci.Home page
M. E. Martone, Y. Z. Jones, S. J. Young, M. H. Ellisman, J. A. Zivin, and B.-R. Hu
Modification of Postsynaptic Densities after Transient Cerebral Ischemia: A Quantitative and Three-Dimensional Ultrastructural Study
J. Neurosci., March 15, 1999; 19(6): 1988 - 1997.
[Abstract] [Full Text] [PDF]


Home page
StrokeHome page
R. P. Wiard, M. C. Dickerson, O. Beek, R. Norton, and B. R. Cooper
Neuroprotective Properties of the Novel Antiepileptic Lamotrigine in a Gerbil Model of Global Cerebral Ischemia
Stroke, March 1, 1995; 26(3): 466 - 472.
[Abstract] [Full Text]


Home page
ScienceHome page
L. Squire and S Zola-Morgan
The medial temporal lobe memory system
Science, September 20, 1991; 253(5026): 1380 - 1386.
[Abstract] [PDF]


Home page
ScienceHome page
L. Squire
Mechanisms of memory
Science, June 27, 1986; 232(4758): 1612 - 1619.
[Abstract] [PDF]