Document Detail


Early postinjury exercise reverses memory deficits and retards the progression of closed-head injury in mice.
MedLine Citation:
PMID:  23184513     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Closed-head injury (CHI) usually involves both physical damage of neurons and neuroinflammation. Although exercise promotes neuronal repair and suppresses neuroinflammation, CHI patients currently often remain resting during the post-traumatic period. This study aimed to investigate whether and how postinjury exercise benefited the brain structure and function in mice after CHI. Closed-head injury immediately caused an elevated neurological severity score, with rapid loss of object recognition memory, followed by progressive location-dependent brain damage (neuronal loss and activation of microglia in the cortex and hippocampus). An early exercise protocol at moderate intensity (starting 2 days postimpact and lasting for 7 or 14 days) effectively restored the object recognition memory and prevented the progressive neuronal loss and activation of microglia. However, if the exercise started 9 days postimpact, it was unable to recover recognition memory deficits. In parallel, early exercise intervention drastically promoted neurite regeneration, while late exercise intervention was much less effective. We also tested the possible involvement of brain-derived neurotrophic factor (BDNF) and mitogen-activated protein kinase phosphatase-1 (MKP-1) in the exercise-induced beneficial effects. Exercise gradually restored the impact-abolished hippocampal expression of BDNF and MPK-1, while oral administration of triptolide (a synthesis inhibitor of MKP-1 and an antagonist of nuclear factor-B) before each bout of exercise blocked the restorative effects of exercise on MKP-1 and recognition memory, as well as the exercise-induced retardation of neuronal loss. Although triptolide treatment alone inhibited activation of microglia and maintained neuronal numbers, it did not recover the injury-hampered recognition memory. Overall, moderate exercise shortly after CHI reversed the deficits in recognition memory and prevented the progression of brain injury.
Authors:
Mei-Feng Chen; Tung-Yi Huang; Yu-Min Kuo; Lung Yu; Hsiun-ing Chen; Chauying J Jen
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-11-26
Journal Detail:
Title:  The Journal of physiology     Volume:  591     ISSN:  1469-7793     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2013 Feb 
Date Detail:
Created Date:  2013-02-18     Completed Date:  2013-08-06     Revised Date:  2014-02-18    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  985-1000     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Brain-Derived Neurotrophic Factor / metabolism
CA1 Region, Hippocampal / cytology,  physiology
Cerebral Cortex / cytology,  physiology
Dual Specificity Phosphatase 1 / metabolism
Head Injuries, Closed / metabolism,  physiopathology,  therapy*
Male
Memory Disorders / metabolism,  physiopathology,  therapy*
Mice
Mice, Inbred ICR
Microglia / physiology
Neurons / physiology
Physical Conditioning, Animal*
Recognition (Psychology)
Chemical
Reg. No./Substance:
0/Brain-Derived Neurotrophic Factor; EC 3.1.3.48/Dual Specificity Phosphatase 1; EC 3.1.3.48/Dusp1 protein, mouse
Comments/Corrections

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