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|Title:||RELATIONSHIP BETWEEN HIPPOCAMPAL DAMAGE AND BEHAVIORAL OUTCOME IN RATS FOLLOWING GLOBAL CEREBRAL ISCHEMIA
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|Authors/Affiliations:||1 Pavel Piterkin*; 1 Emily Cole; 1 Ana Gamliel ; 1 Stephane Gaskin; 2 Sara-Claude Michon; 1 Marilyn Tardif; 1 Angela Vavassis; 1 Dave G. Mumby; |
1 Concordia University, Montreal, QC, Canada; 2 Rush University, Chicago, USA.
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|Content:||Objective: Memory impairments following global cerebral ischemia have traditionally been associated with damage to the hippocampal formation, but some ensuing impairments, such as object-recognition deficits, suggest the presence of extra-hippocampal neuropathology. The goal of the present study was to determine whether hippocampal damage induced by global cerebral ischemia is related to rats’ performance on allocentric spatial memory and object recognition tasks. |
Materials and Methods: Global cerebral ischemia was induced using the four-vessel occlusion procedure. All rats underwent permanent occlusion of the vertebral arteries and rats in the experimental condition underwent 15-minute occlusion of the common carotid arteries. Following a recovery period rats’ allocentric spatial memory was assessed using the delayed matching-to-place (DMTP) task conducted in the water maze; recognition memory was assessed using the novel-object-preference (NOP) test of object recognition. Upon completion of behavioral testing, hippocampal integrity was examined by visual quantification of Nissl-stained neurons, as well as immunocytochemical staining for astrogliosis (glial fibrillary acidic protein expression), and alterations in cytoskeletal structure (microtubule-associated protein 2 expression).
Results: Ischemic rats were impaired relative to controls on both, allocentric spatial memory and object recognition tasks. Examination of Nissl stained sections revealed considerable cell loss in the post-ischemic hippocampus and immunocytochemical assays demonstrated group differences as well. Correlational analyses revealed a relationship between hippocampal damage and DMTP performance following global cerebral ischemia, but no relationship between histological outcome and object recognition impairments was apparent.
Conclusions: These results support the premise that ischemia induced neuropathology in the hippocampus cannot exclusively account for the entire range of mnemonic deficits that accompany this cardiovascular insult.
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