Siriluk Somredngan1, Wachiryah Thong-Asa1. 1. Animal Toxicology and Physiology Specialty Research Unit (ATPSRU), Department of Zoology, Faculty of Science, Kasetsart University, Bangkok, Thailand.
Abstract
BACKGROUND: Chronic cerebral hypoperfusion (CCH) is associated with neurological changes and cognitive decline. It is a major cause of vascular dementia and a contributing factor in Alzheimer disease. Animal models are useful in helping to elucidate the mechanisms of these diseases while demonstrating differences in pathological onset and severity. Furthermore, different mouse strains show differences in their susceptibility to neurological damage resulting in different cognitive outcomes. PURPOSE: This study investigated the effect of CCH induced by permanent unilateral common carotid artery occlusion (UCO) on neurological damage in vulnerable brain regions such as hippocampus, striatum, and white matter areas from 2 to 8 weeks following CCH induction. METHODS: Thirty-six male Institute of Cancer Research (ICR) mice were randomly divided into 2 main experimental groups, Sham and UCO. These 2 main groups were further divided into 3 observation periods of 2, 4, and 8 weeks following CCH. Histological study was then employed using 0.1% cresyl violet and luxol fast blue staining to assess neurological damage. RESULTS: We found equal levels of neurological damage induced by CCH between ipsi- and contralateral hemispheres. Hippocampus and striatum damage were slightly increased from 2 to 8 weeks rising to significance at 8 weeks in both areas, while the white matter densities of the corpus callosum, internal capsule, optic tract and striatum fiber did not change. CONCLUSION: CCH induced by UCO in ICR mice induces hippocampal and striatal damage at 8 weeks while leaving white matter undamaged.
BACKGROUND: Chronic cerebral hypoperfusion (CCH) is associated with neurological changes and cognitive decline. It is a major cause of vascular dementia and a contributing factor in Alzheimer disease. Animal models are useful in helping to elucidate the mechanisms of these diseases while demonstrating differences in pathological onset and severity. Furthermore, different mouse strains show differences in their susceptibility to neurological damage resulting in different cognitive outcomes. PURPOSE: This study investigated the effect of CCH induced by permanent unilateral common carotid artery occlusion (UCO) on neurological damage in vulnerable brain regions such as hippocampus, striatum, and white matter areas from 2 to 8 weeks following CCH induction. METHODS: Thirty-six male Institute of Cancer Research (ICR) mice were randomly divided into 2 main experimental groups, Sham and UCO. These 2 main groups were further divided into 3 observation periods of 2, 4, and 8 weeks following CCH. Histological study was then employed using 0.1% cresyl violet and luxol fast blue staining to assess neurological damage. RESULTS: We found equal levels of neurological damage induced by CCH between ipsi- and contralateral hemispheres. Hippocampus and striatum damage were slightly increased from 2 to 8 weeks rising to significance at 8 weeks in both areas, while the white matter densities of the corpus callosum, internal capsule, optic tract and striatum fiber did not change. CONCLUSION: CCH induced by UCO in ICR mice induces hippocampal and striatal damage at 8 weeks while leaving white matter undamaged.
Entities:
Keywords:
Chronic cerebral hypoperfusion; Hippocampus; Striatum; Unilateral common carotid artery occlusion; White matter
Authors: B C White; J M Sullivan; D J DeGracia; B J O'Neil; R W Neumar; L I Grossman; J A Rafols; G S Krause Journal: J Neurol Sci Date: 2000-10-01 Impact factor: 3.181