A Mouse Model for Chronic Cerebral Hypoperfusion-induced Cognitive Dysfunction

Abstract

Background: Chronic cerebral hypoperfusion potentially contributes to the initiation and progression of vascular dementia (VD). Bilateral common carotid artery occlusion (two-vessel occlusion) is the most commonly used animal model to replicate this pathological condition but with high mortality and severe histological cerebral damage. Unilateral common carotid artery occlusion (one-vessel occlusion) was introduced to simulate clinical conditions. Our study was designed to further characterize this model.Methods: In this study, eight-week old CD-1 mice were subjected to left common carotid artery occlusion (LCCAO). Two weeks after the occlusion, their learning and memory were assessed by Barnes maze and fear conditioning. Histo-morphological changes were evaluated by Hematoxylin-Eosin staining. Neuronal and axonal degenerative changes were examined by amino-cupric sliver staining.Results: LCCAO increased the time to find the target box in the Barnes maze test during the 4-day training sessions and one day after the training sessions compared with sham group mice. There was no difference in context-related or tone-related freezing behavior between these two groups. No significant histological neuronal cell damage or degeneration was observed in brain sections of hippocampus and corpus callosum in these two groups.Conclusions: Our results suggest that LCCAO can be used to mimic the vascular dementia. Citation: Jun Li, Zhi-Yi Zuo. A mouse model for chronic cerebral hypoperfusion-induced cognitive dysfunction. J Anesth Perioper Med 2017; 4: 60-66. doi:10.24015/JAPM.2017.0015This is an open-access article, published by Evidence Based Communications (EBC). This work is licensed under the Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution, and reproduction in any medium or format for any lawful purpose. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.