Abstract
Memory impairment is commonly noted in stroke survivors, and can lead to delay of functional recovery. Exercise has been proved to improve memory in adult healthy subjects. Such beneficial effects are often suggested to relate to hippocampal synaptic plasticity, which is important for memory processing. Previous evidence showed that in normal rats, low intensity exercise can improve synaptic plasticity better than high intensity exercise. However, the effects of exercise intensities on hippocampal synaptic plasticity and spatial memory after brain ischemia remain unclear. In this study, we investigated such effects in brain ischemic rats. The middle cerebral artery occlusion (MCAO) procedure was used to induce brain ischemia. After the MCAO procedure, rats were randomly assigned to sedentary (Sed), low-intensity exercise (Low-Ex), or high-intensity exercise (High-Ex) group. Treadmill training began from the second day post MCAO procedure, 30 min/day for 14 consecutive days for the exercise groups. The Low-Ex group was trained at the speed of 8 m/min, while the High-Ex group at the speed of 20 m/min. The spatial memory, hippocampal brain-derived neurotrophic factor (BDNF), synapsin-I, postsynaptic density protein 95 (PSD-95), and dendritic structures were examined to document the effects. Serum corticosterone level was also quantified as stress marker. Our results showed the Low-Ex group, but not the High-Ex group, demonstrated better spatial memory performance than the Sed group. Dendritic complexity and the levels of BDNF and PSD-95 increased significantly only in the Low-Ex group as compared with the Sed group in bilateral hippocampus. Notably, increased level of corticosterone was found in the High-Ex group, implicating higher stress response. In conclusion, after brain ischemia, low intensity exercise may result in better synaptic plasticity and spatial memory performance than high intensity exercise; therefore, the intensity is suggested to be considered during exercise training.
Highlights
Memory deficits are frequently noted after stroke, and are often related to impaired hippocampal function [1]
Running exercise has been proved to increase the expressions of hippocampal brainderived neurotrophic factor (BDNF) and synapsin-I, which contribute to the spatial memory performance in normal rats [12]
Group differences were observed (p,.05) and post-hoc test revealed rats in the low-intensity exercise (Low-Ex) group spent longer time in the training quadrant compared with the Sed group (P,.05)
Summary
Memory deficits are frequently noted after stroke, and are often related to impaired hippocampal function [1]. Exercise was found to improve memory performance in transient global ischemic rat models [5] The mechanisms underlying such beneficial effects on memory are often related to the hippocampal synaptic plasticity [6]. Running exercise has been proved to increase the expressions of hippocampal BDNF and synapsin-I, which contribute to the spatial memory performance in normal rats [12]. Dendritic morphological changes, such as increase dendritic aborization and dendritic spine density, have been reported after physical exercise [13]. The effects of exercise intensity on hippocampal synaptic plasticity and spatial memory after brain ischemia remain unclear
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