• H Jeon, J Ai, M Sabri, A Tariq, and R L Macdonald.
• Division of Neurosurgery, St. Michael's Hospital, Keenan Research Centre, Li Ka Shing Knowledge Institute of St. Michael's Hospital and Department of Surgery, University of Toronto, Ontario, Canada.
• Neuroscience. 2010 Sep 15; 169 (4): 1805-14.

AbstractAbout 50% of subarachnoid hemorrhage (SAH) survivors have cognitive or neurobehavioral dysfunction. The mechanisms are not known. This study characterized behavioral deficits in a rat SAH model, and correlated these changes with histological alterations. SAH was induced by injection of 0.3 ml blood into the prechiasmatic cistern. Cognitive and memory changes were investigated in the Morris water maze. Neuronal cell death was evaluated by fluoro-jade and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. Vasospasm was assessed on cross-sections of middle and anterior cerebral arteries. Microthromboemboli were quantified by fibrinogen staining. Escape latency and swimming distance were significantly increased in rats with SAH as compared to controls (P<0.05-0.001). SAH rats tended to do poorly on accuracy in spatial and working memory tests. SAH rats had a significantly higher number of fluoro-jade and TUNEL positive neurons in CA1 and CA3 of the hippocampus, cerebral cortex and Purkinje cells in the cerebellum (P<0.05-0.001). The number of microthromboemboli in the cortex and cerebellum were significantly higher after SAH than in controls (P<0.05-0.001). Cognitive deficits were induced by SAH in rats. There was a significant increase in apoptotic neurons in all regions of brain examined. However, cell death in the hippocampus was not sufficient to cause the neurobehavioral deficits observed in the Morris water maze. This suggests that other factors such as dysfunction of neurotransmission or plasticity in hippocampal pathways might contribute to the impairments.(c) 2010 IBRO. Published by Elsevier Ltd. All rights reserved.

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