Document Detail


Regular voluntary exercise cures stress-induced impairment of cognitive function and cell proliferation accompanied by increases in cerebral IGF-1 and GST activity in mice.
MedLine Citation:
PMID:  20307585     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Chronic stress impairs cognitive function and hippocampal neurogenesis. This impairment is attributed to increases in oxidative stress, which result in the accumulation of lipid peroxide. On the other hand, voluntary exercise enhances cognitive function, hippocampal neurogenesis, and antioxidant capacity in normal animals. However, the effects of voluntary exercise on cognitive function, neurogenesis, and antioxidants in stressed mice are unclear. This study was designed to investigate whether voluntary exercise cures stress-induced impairment of cognitive function accompanied by improvement of hippocampal neurogenesis and increases in antioxidant capacity. Stressed mice were exposed to chronic restraint stress (CRS), which consisted of 12h immobilization daily and feeding in a small cage, for 8 weeks. Exercised mice were allowed free access to a running wheel during their exposure to CRS. At the 6th week, cognitive function was examined using the Morris water maze (MWM) test. Daily voluntary exercise restored stress-induced impairment of cognitive function and the hippocampal cell proliferation of newborn cells but not cell survival. Voluntary exercise increased insulin-like growth factor 1 (IGF-1) protein and mRNA expression in the cerebral cortex and liver, respectively. In addition, CRS resulted in a significant increase in the number of 4-hydrosynonenal (4-HNE)-positive cells in the hippocampal dentate gyrus; whereas, voluntary exercise inhibited it and enhanced glutathione s-transferases (GST) activity in the brain. These findings suggest that voluntary exercise attenuated the stress-induced impairment of cognitive function accompanied by improvement of cell proliferation in the dentate gyrus. This exercise-induced improvement was attributed to exercise-induced enhancement of IGF-1 protein and GST activity in the brain.
Authors:
Sanae Nakajima; Ikuroh Ohsawa; Shigeo Ohta; Makoto Ohno; Toshio Mikami
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-03-20
Journal Detail:
Title:  Behavioural brain research     Volume:  211     ISSN:  1872-7549     ISO Abbreviation:  Behav. Brain Res.     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-05-03     Completed Date:  2010-08-03     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8004872     Medline TA:  Behav Brain Res     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  178-84     Citation Subset:  IM    
Copyright Information:
Copyright 2010 Elsevier B.V. All rights reserved.
Affiliation:
Department of Biochemistry and Cell Biology, Institute of Gerontology, Nippon Medical School, Kawasaki, Kanagawa 211-8533, Japan.
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MeSH Terms
Descriptor/Qualifier:
Adaptation, Physiological
Animals
Cell Proliferation
Cerebral Cortex / cytology,  metabolism
Cognition / physiology
Dentate Gyrus / cytology*,  physiology
Glutathione Transferase / metabolism*
Hippocampus / cytology,  physiology*
Insulin-Like Growth Factor I / genetics,  metabolism*
Liver / metabolism
Male
Maze Learning / physiology*
Mice
Mice, Inbred C57BL
Neurogenesis / physiology
Physical Conditioning, Animal / physiology*
RNA, Messenger / analysis
Random Allocation
Stress, Psychological / metabolism
Chemical
Reg. No./Substance:
0/RNA, Messenger; 67763-96-6/Insulin-Like Growth Factor I; EC 2.5.1.18/Glutathione Transferase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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