Chronic stress prior to hippocampal stroke enhances post-stroke spatial deficits in the ziggurat task

► Stress history impaired the hippocampal function in the ziggurat task after stroke. ► Pre-stroke stress also induced enhanced tissue loss in the hippocampus. ► These effects have not been found with treatment with corticosterone alone. ► Dorsal and ventral hippocampus may respond differently to st...

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Published inNeurobiology of learning and memory Vol. 95; no. 3; pp. 335 - 345
Main Authors Faraji, Jamshid, Ejaredar, Maede, Metz, Gerlinde A., Sutherland, Robert J.
Format Journal Article
LanguageEnglish
Published Amsterdam Elsevier Inc 01.03.2011
Elsevier
Elsevier BV
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Summary:► Stress history impaired the hippocampal function in the ziggurat task after stroke. ► Pre-stroke stress also induced enhanced tissue loss in the hippocampus. ► These effects have not been found with treatment with corticosterone alone. ► Dorsal and ventral hippocampus may respond differently to stress experiences. Stress is one of the most important variables to determine recovery following stroke. We have previously reported that post-stroke exposure to either stress or corticosterone (CORT) alleviates hippocampal ischemic outcome. The present experiment expands previous findings by investigating the influence of exposure to stress prior to ischemic event. Rats received either daily restraint stress (1h/day; 16 consecutive days) or CORT (0.5mg/kg; 16 consecutive days) prior to focal ischemic stroke in the hippocampus induced by bilateral injection of endothelin-1 (ET-1). All experimental groups were then tested in the ziggurat task, a new task for spatial cognition. The stress+stroke group showed significant deficits in both hippocampal structure and function. No deleterious effect of pre-stroke exposure to CORT was found in the CORT+stroke group. Our results indicate that a history of chronic stress sensitizes hippocampal cells to the damaging consequences of focal ischemia. The opposing effects of CORT-related experiences in this study not only reflect the diversity of glucocorticoid actions in the stress response, but also provide evidence that elevated CORT in the absence of emotional disturbance is not sufficient to produce hippocampal deficit.
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ISSN:1074-7427
1095-9564
DOI:10.1016/j.nlm.2011.01.006