PMID- 23184513
OWN - NLM
STAT- MEDLINE
DCOM- 20130806
LR  - 20211021
IS  - 1469-7793 (Electronic)
IS  - 0022-3751 (Print)
IS  - 0022-3751 (Linking)
VI  - 591
IP  - 4
DP  - 2013 Feb 15
TI  - Early postinjury exercise reverses memory deficits and retards the progression of 
      closed-head injury in mice.
PG  - 985-1000
LID - 10.1113/jphysiol.2012.241125 [doi]
AB  - 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.
FAU - Chen, Mei-Feng
AU  - Chen MF
AD  - Institute of Basic Medical Sciences, National Cheng Kung University Medical 
      College, Tainan, Taiwan.
FAU - Huang, Tung-Yi
AU  - Huang TY
FAU - Kuo, Yu-Min
AU  - Kuo YM
FAU - Yu, Lung
AU  - Yu L
FAU - Chen, Hsiun-ing
AU  - Chen HI
FAU - Jen, Chauying J
AU  - Jen CJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20121126
PL  - England
TA  - J Physiol
JT  - The Journal of physiology
JID - 0266262
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - EC 3.1.3.48 (Dual Specificity Phosphatase 1)
RN  - EC 3.1.3.48 (Dusp1 protein, mouse)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - CA1 Region, Hippocampal/cytology/physiology
MH  - Cerebral Cortex/cytology/physiology
MH  - Dual Specificity Phosphatase 1/metabolism
MH  - Head Injuries, Closed/metabolism/physiopathology/*therapy
MH  - Male
MH  - Memory Disorders/metabolism/physiopathology/*therapy
MH  - Mice
MH  - Mice, Inbred ICR
MH  - Microglia/physiology
MH  - Neurons/physiology
MH  - *Physical Conditioning, Animal
MH  - Recognition, Psychology
PMC - PMC3591710
EDAT- 2012/11/28 06:00
MHDA- 2013/08/07 06:00
PMCR- 2014/02/15
CRDT- 2012/11/28 06:00
PHST- 2012/11/28 06:00 [entrez]
PHST- 2012/11/28 06:00 [pubmed]
PHST- 2013/08/07 06:00 [medline]
PHST- 2014/02/15 00:00 [pmc-release]
AID - jphysiol.2012.241125 [pii]
AID - 10.1113/jphysiol.2012.241125 [doi]
PST - ppublish
SO  - J Physiol. 2013 Feb 15;591(4):985-1000. doi: 10.1113/jphysiol.2012.241125. Epub 
      2012 Nov 26.