Document Detail

Voluntary exercise protects against stress-induced decreases in brain-derived neurotrophic factor protein expression.
MedLine Citation:
PMID:  15026138     Owner:  NLM     Status:  MEDLINE    
Exercise is increasingly recognized as an intervention that can reduce CNS dysfunctions such as cognitive decline, depression and stress. Previously we have demonstrated that brain-derived neurotrophic factor (BDNF) is increased in the hippocampus following exercise. In this study we tested the hypothesis that exercise can counteract a reduction in hippocampal BDNF protein caused by acute immobilization stress. Since BDNF expression is suppressed by corticosterone (CORT), circulating CORT levels were also monitored. In animals subjected to 2 h immobilization stress, CORT was elevated immediately following, and at 1 h after the cessation of stress, but remained unchanged from baseline up to 24 h post-stress. The stress protocol resulted in a reduction in BDNF protein at 5 and 10 h post-stress that returned to baseline at 24 h. To determine if exercise could prevent this stress-induced reduction in BDNF protein, animals were given voluntary access to running wheels for 3 weeks prior to the stress. Stressed animals, in the absence of exercise, again demonstrated an initial elevation in CORT (at 0 h) and a subsequent decrease in hippocampal BDNF at the 10 h time point. Exercising animals, both non-stressed and stressed, demonstrated circulating CORT and hippocampal BDNF protein levels that were significantly elevated above control values at both time points examined (0 and 10 h post-stress). Thus, the persistently high CORT levels in exercised animals did not affect the induction of BDNF with exercise, and the effect of immobilization stress on BDNF protein was overcome. To examine the role of CORT in the stress-related regulation of BDNF protein, experiments were carried out in adrenalectomized (ADX) animals. BDNF protein was not downregulated as a result of immobilization stress in ADX animals, while there continued to be an exercise-induced upregulation of BDNF. This study demonstrates that CORT modulates stress-related alterations in BDNF protein. Further, exercise can override the negative effects of stress and high levels of CORT on BDNF protein. Voluntary physical activity may, therefore, represent a simple non-pharmacological tool for the maintenance of neurotrophin levels in the brain.
P A Adlard; C W Cotman
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Neuroscience     Volume:  124     ISSN:  0306-4522     ISO Abbreviation:  Neuroscience     Publication Date:  2004  
Date Detail:
Created Date:  2004-03-17     Completed Date:  2004-06-08     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  7605074     Medline TA:  Neuroscience     Country:  United States    
Other Details:
Languages:  eng     Pagination:  985-92     Citation Subset:  IM    
Institute for Brain Aging and Dementia, 1113 Gillespie N.R.F., University of California, Irvine, Irvine, CA 92697-4540, USA.
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MeSH Terms
Acute Disease
Brain / metabolism*
Brain-Derived Neurotrophic Factor / metabolism*
Corticosterone / metabolism
Mice, Inbred C57BL
Motor Activity / physiology*
Stress, Physiological / etiology,  metabolism*
Time Factors
Grant Support
AG-13411-04/AG/NIA NIH HHS
Reg. No./Substance:
0/Brain-Derived Neurotrophic Factor; 50-22-6/Corticosterone

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