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A Low Mortality Rat Model to Assess Delayed Cerebral Vasospasm After Experimental Subarachnoid Hemorrhage
Published on: January 17, 2013
Learning deficits after experimental subarachnoid hemorrhage in rats
1Division 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
|July 6, 2010
Summary
Subarachnoid hemorrhage (SAH) in rats caused cognitive and memory deficits. While SAH increased neuronal apoptosis, hippocampus cell death alone did not explain these neurobehavioral impairments.
Area of Science:
- Neuroscience
- Pathology
Background:
- Subarachnoid hemorrhage (SAH) survivors frequently experience cognitive and neurobehavioral dysfunction.
- The underlying mechanisms contributing to these deficits remain largely unknown.
Purpose of the Study:
- To characterize behavioral deficits in a rat model of SAH.
- To correlate these behavioral changes with histological alterations in the brain.
Main Methods:
- SAH was induced in rats via blood injection into the prechiasmatic cistern.
- Cognitive and memory functions were assessed using the Morris water maze.
- Neuronal cell death was quantified using fluoro-jade and TUNEL staining.
- Vasospasm and microthromboemboli were evaluated through histological analysis.
Main Results:
- SAH rats exhibited significantly increased escape latency and swimming distance in the Morris water maze.
- SAH rats showed impaired spatial and working memory accuracy.
- A significant increase in apoptotic neurons was observed in the hippocampus, cerebral cortex, and cerebellum of SAH rats.
- Elevated levels of microthromboemboli were detected in the cortex and cerebellum post-SAH.
Conclusions:
- SAH induces significant cognitive and memory deficits in rats.
- Increased neuronal apoptosis occurs throughout the brain following SAH.
- Hippocampal cell death alone is insufficient to account for the observed cognitive impairments, suggesting other contributing factors like neurotransmission or plasticity dysfunction.
