2013Unpublished venueRequires access

Cognitive impairment and changes of neuronal plasticity in rats of chronic cerebral hypoperfusion

Fei Yu

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Abstract

Objective A new cerebral arteriovenous malformations ( AVMs) rat model was developed to study the effect of chronic cerebral hypoperfusion on cognitive function and neuronal plasticity in rats. Methods Agedmatched animals comprised a control group. Three months after surgery,Morris water waze test was performed to evaluate the cognitive function in rats. Neuronal plasticity was assessed by measuring the protein expression of MAP-2, GAP-43 and synaptophysin in the hippocampal regions of rats with immunohistochemistry and western blotting. Results The average time of escape latency was significantly longer in the model rats than that in the control rats,and both the time spent in the platform quadrant and the frequency of original platform crossing during space probe trials were less than those in the control animals. The expression levels of MAP-2 and synaptophysin protein in hippocampal areas in the model rats were less than those in the control rats. However,there was no difference on the GAP-43 expression between the two groups. Conclusion These data suggested that chronic cerebral hypoperfusion associated with AVMs could lead to cognitive impairment in rats,which may be partially explained by reduced expression of MAP-2 and synaptophysin at the protein level in the hippocampal area.

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Objective A new cerebral arteriovenous malformations ( AVMs) rat model was developed to study the effect of chronic cerebral hypoperfusion on cognitive function and neuronal plasticity in rats. Methods Agedmatched animals comprised a control group. Three months after surgery,Morris water waze test was performed to evaluate the cognitive function in rats. Neuronal plasticity was assessed by measuring the protein expression of MAP-2, GAP-43 and synaptophysin in the hippocampal regions of rats with immunohistochemistry and western blotting. Results The average time of escape latency was significantly longer in the model rats than that in the control rats,and both the time spent in the platform quadrant and the frequency of original platform crossing during space probe trials were less than those in the control animals. The expression levels of MAP-2 and synaptophysin protein in hippocampal areas in the model rats were less than those in the control rats. However,there was no difference on the GAP-43 expression between the two groups. Conclusion These data suggested that chronic cerebral hypoperfusion associated with AVMs could lead to cognitive impairment in rats,which may be partially explained by reduced expression of MAP-2 and synaptophysin at the protein level in the hippocampal area.

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Available abstract

Objective A new cerebral arteriovenous malformations ( AVMs) rat model was developed to study the effect of chronic cerebral hypoperfusion on cognitive function and neuronal plasticity in rats. Methods Agedmatched animals comprised a control group. Three months after surgery,Morris water waze test was performed to evaluate the cognitive function in rats. Neuronal plasticity was assessed by measuring the protein expression of MAP-2, GAP-43 and synaptophysin in the hippocampal regions of rats with immunohistochemistry and western blotting. Results The average time of escape latency was significantly longer in the model rats than that in the control rats,and both the time spent in the platform quadrant and the frequency of original platform crossing during space probe trials were less than those in the control animals. The expression levels of MAP-2 and synaptophysin protein in hippocampal areas in the model rats were less than those in the control rats. However,there was no difference on the GAP-43 expression between the two groups. Conclusion These data suggested that chronic cerebral hypoperfusion associated with AVMs could lead to cognitive impairment in rats,which may be partially explained by reduced expression of MAP-2 and synaptophysin at the protein level in the hippocampal area.

Key concepts: Synaptophysin, Hippocampal formation, Hippocampus, Morris water navigation task, Neuroplasticity, Neuroscience, Perfusion, Synaptic plasticity

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