Aerobic Exercise Alleviates Ischemia-Induced Memory Impairment by Enhancing Cell Proliferation and Suppressing Neuronal Apoptosis in Hippocampus
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Purpose: Neurogenic lower urinary tract dysfunction (NLUTD) is a possible consequence of several neurological disorders. NLUTD may produce debilitating symptoms and serious complications, such as chronic renal failure, and recurrent urinarytract infections. Many animal studies of NLUTD symptoms have focused on animal models of cerebral ischemia. In the presentstudy, we investigated the effects of treadmill exercise on memory function and its relation to cell proliferation and apoptosisin the hippocampus, following transient global ischemia in gerbils. Methods: To induce transient global ischemia in gerbil, both common carotid arteries were occluded for 5 minutes. Gerbils inthe exercise groups were forced to run on a treadmill exercise for 30 minutes once a day for 2 weeks. Step-down avoidancetask and Y maze task were performed. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL)-staining, immunohistochemistry for 5-bromo-2ʹ-deoxyridine, doublecortin, caspase-3, and Western blot for brain-derivedneurotrophic factor (BDNF), Bax, Bcl-2, cytochrome c, caspase-3 were conducted. Results: Ischemia caused memory impairment with an increase of cell proliferation, BDNF expression, and apoptosis in thehippocampus. Treadmill exercise improved memory function with further increase of cell proliferation and BDNF expressionand a decrease of apoptosis. Conclusions: The animal model that we have developed and our assessment of the relation between exercise and brain functioncan be useful tools for future investigations of NLUTD symptoms associated with stroke, particularly ischemic stroke. Thepresent study suggests that treadmill exercise promoted the recovery of brain function after cerebral ischemia.
Abstract
Purpose: Neurogenic lower urinary tract dysfunction (NLUTD) is a possible consequence of several neurological disorders. NLUTD may produce debilitating symptoms and serious complications, such as chronic renal failure, and recurrent urinarytract infections. Many animal studies of NLUTD symptoms have focused on animal models of cerebral ischemia. In the presentstudy, we investigated the effects of treadmill exercise on memory function and its relation to cell proliferation and apoptosisin the hippocampus, following transient global ischemia in gerbils. Methods: To induce transient global ischemia in gerbil, both common carotid arteries were occluded for 5 minutes. Gerbils inthe exercise groups were forced to run on a treadmill exercise for 30 minutes once a day for 2 weeks. Step-down avoidancetask and Y maze task were performed. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL)-staining, immunohistochemistry for 5-bromo-2ʹ-deoxyridine, doublecortin, caspase-3, and Western blot for brain-derivedneurotrophic factor (BDNF), Bax, Bcl-2, cytochrome c, caspase-3 were conducted. Results: Ischemia caused memory impairment with an increase of cell proliferation, BDNF expression, and apoptosis in thehippocampus. Treadmill exercise improved memory function with further increase of cell proliferation and BDNF expressionand a decrease of apoptosis. Conclusions: The animal model that we have developed and our assessment of the relation between exercise and brain functioncan be useful tools for future investigations of NLUTD symptoms associated with stroke, particularly ischemic stroke. Thepresent study suggests that treadmill exercise promoted the recovery of brain function after cerebral ischemia.
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