Dendritic morphology of neurons in medial prefrontal cortex and hippocampus in 2VO rats.

Cerebral ischemia is the main cause of cognitive impairment. Changes in dendritic morphology and spines have been shown to occur with synaptic plasticity and cognitive function. Bilateral occlusion of the common carotid arteries (2VO) in rats was an effective model of chronic cerebral ischemia. In this experiment, SD rats were divided into model group (2VO) and sham-operated group. At 2, 4, 8 and 16 weeks, rats were tested in Morris water maze to observe learning and memory abilities, and then the brain tissue was stained by Golgi method to investigate the morphology of dendrites of pyramidal neurons under light microscope. Dendritic length and arborization and spine density of pyramidal neurons in medial prefrontal cortex (mPFC) and hippocampal CA1 were analyzed by ImageJ. Progressive learning and memory deficits appeared since 2 weeks. Compared to the sham-operated group, the dendritic length and arborization significantly decreased in the model group at 4, 8 and 16 weeks after 2VO in CA1, while there was no significant difference in mPFC. Dendritic spine density in hippocampal CA1 of the model group significantly decreased after 2 weeks, and it was decreased after 8 weeks in mPFC. The results suggest that under the condition of chronic cerebral ischemia, the alteration of dendritic morphology and spine density underlay cognitive impairment.