PMID- 30941019
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200930
IS  - 1662-5102 (Print)
IS  - 1662-5102 (Electronic)
IS  - 1662-5102 (Linking)
VI  - 13
DP  - 2019
TI  - Wheel Running Improves Motor Function and Spinal Cord Plasticity in Mice With 
      Genetic Absence of the Corticospinal Tract.
PG  - 106
LID - 10.3389/fncel.2019.00106 [doi]
LID - 106
AB  - Our previous studies showed that mutant mice with congenital absence of the 
      corticospinal tract (CST) undergo spontaneous remodeling of motor networks to 
      partially compensate for absent CST function. Here, we asked whether voluntary 
      wheel running could further improve locomotor plasticity in CST-deficient mice. 
      Adult mutant mice were randomly allocated to a "runners" group with free access 
      to a wheel, or a "non-runners" group with no access to a wheel. In comparison 
      with non-runners, there was a significant motor improvement including fine 
      movement, grip strength, decreased footslip errors in runners after 8-week 
      training, which was supported by the elevated amplitude of electromyography 
      recording and increased neuromuscular junctions in the biceps. In runners, 
      terminal ramifications of monoaminergic and rubrospinal descending axons were 
      significantly increased in spinal segments after 12 weeks of exercise compared to 
      non-runners. 5-ethynyl-2'-deoxyuridine (EDU) labeling showed that proliferating 
      cells, 90% of which were Olig2-positive oligodendrocyte progenitors, were 
      4.8-fold more abundant in runners than in non-runners. In 8-week runners, RNAseq 
      analysis of spinal samples identified 404 genes up-regulated and 398 genes 
      down-regulated, and 69 differently expressed genes involved in signal 
      transduction, among which the NF-kappaB, PI3K-Akt and cyclic AMP (cAMP) signaling 
      were three top pathways. Twelve-week training induced a significant elevation of 
      postsynaptic density protein 95 (PSD95), synaptophysin 38 and myelin basic 
      protein (MBP), but not of brain derived neurotrophic factor (BDNF), glial cell 
      line-derived neurotrophic factor (GDNF) and insulin like growth factor-1 (IGF-1). 
      Thus, locomotor training activates multiple signaling pathways, contributes to 
      neural plasticity and functional improvement, and might palliate locomotor 
      deficits in patients.
FAU - Zhang, Wei
AU  - Zhang W
AD  - Guangdong-Hongkong-Macau Institute of CNS Regeneration, Ministry of Education CNS 
      Regeneration Collaborative Joint Laboratory, Jinan University, Guangzhou, China.
FAU - Yang, Bin
AU  - Yang B
AD  - Guangdong-Hongkong-Macau Institute of CNS Regeneration, Ministry of Education CNS 
      Regeneration Collaborative Joint Laboratory, Jinan University, Guangzhou, China.
FAU - Weng, Huandi
AU  - Weng H
AD  - Guangdong-Hongkong-Macau Institute of CNS Regeneration, Ministry of Education CNS 
      Regeneration Collaborative Joint Laboratory, Jinan University, Guangzhou, China.
FAU - Liu, Tao
AU  - Liu T
AD  - Guangdong-Hongkong-Macau Institute of CNS Regeneration, Ministry of Education CNS 
      Regeneration Collaborative Joint Laboratory, Jinan University, Guangzhou, China.
FAU - Shi, Lingling
AU  - Shi L
AD  - Guangdong-Hongkong-Macau Institute of CNS Regeneration, Ministry of Education CNS 
      Regeneration Collaborative Joint Laboratory, Jinan University, Guangzhou, China.
FAU - Yu, Panpan
AU  - Yu P
AD  - Guangdong-Hongkong-Macau Institute of CNS Regeneration, Ministry of Education CNS 
      Regeneration Collaborative Joint Laboratory, Jinan University, Guangzhou, China.
FAU - So, Kwok-Fai
AU  - So KF
AD  - Guangdong-Hongkong-Macau Institute of CNS Regeneration, Ministry of Education CNS 
      Regeneration Collaborative Joint Laboratory, Jinan University, Guangzhou, China.
FAU - Qu, Yibo
AU  - Qu Y
AD  - Guangdong-Hongkong-Macau Institute of CNS Regeneration, Ministry of Education CNS 
      Regeneration Collaborative Joint Laboratory, Jinan University, Guangzhou, China.
FAU - Zhou, Libing
AU  - Zhou L
AD  - Guangdong-Hongkong-Macau Institute of CNS Regeneration, Ministry of Education CNS 
      Regeneration Collaborative Joint Laboratory, Jinan University, Guangzhou, China.
AD  - Co-innovation Center of Neuroregeneration, Nantong University, Jiangsu, China.
AD  - Key Laboratory of Neuroscience, School of Basic Medical Sciences, Institute of 
      Neuroscience, The Second Affiliated Hospital, Guangzhou Medical University, 
      Guangzhou, China.
LA  - eng
PT  - Journal Article
DEP - 20190319
PL  - Switzerland
TA  - Front Cell Neurosci
JT  - Frontiers in cellular neuroscience
JID - 101477935
PMC - PMC6433830
OTO - NOTNLM
OT  - animal model
OT  - corticospinal tract
OT  - exercise
OT  - neural plasticity
OT  - oligodendrogenesis
OT  - transcriptomics
EDAT- 2019/04/04 06:00
MHDA- 2019/04/04 06:01
PMCR- 2019/01/01
CRDT- 2019/04/04 06:00
PHST- 2019/02/11 00:00 [received]
PHST- 2019/03/04 00:00 [accepted]
PHST- 2019/04/04 06:00 [entrez]
PHST- 2019/04/04 06:00 [pubmed]
PHST- 2019/04/04 06:01 [medline]
PHST- 2019/01/01 00:00 [pmc-release]
AID - 10.3389/fncel.2019.00106 [doi]
PST - epublish
SO  - Front Cell Neurosci. 2019 Mar 19;13:106. doi: 10.3389/fncel.2019.00106. 
      eCollection 2019.