PMID- 25687543
OWN - NLM
STAT- MEDLINE
DCOM- 20151102
LR  - 20220316
IS  - 1872-6623 (Electronic)
IS  - 0304-3959 (Linking)
VI  - 156
IP  - 3
DP  - 2015 Mar
TI  - Exercise therapy normalizes BDNF upregulation and glial hyperactivity in a mouse 
      model of neuropathic pain.
PG  - 504-513
LID - 10.1097/01.j.pain.0000460339.23976.12 [doi]
AB  - Treatment of neuropathic pain is a clinical challenge likely because of the 
      time-dependent changes in many neurotransmitter systems, growth factors, ionic 
      channels, membrane receptors, transcription factors, and recruitment of different 
      cell types. Conversely, an increasing number of reports have shown the ability of 
      extended and regular physical exercise in alleviating neuropathic pain throughout 
      a wide range of mechanisms. In this study, we investigate the effect of swim 
      exercise on molecules associated with initiation and maintenance of nerve 
      injury-induced neuropathic pain. BALB/c mice were submitted to partial ligation 
      of the sciatic nerve followed by a 5-week aerobic exercise program. Physical 
      training reversed mechanical hypersensitivity, which lasted for an additional 4 
      weeks after exercise interruption. Swim exercise normalized nerve injury-induced 
      nerve growth factor, and brain-derived neurotrophic factor (BDNF) enhanced 
      expression in the dorsal root ganglion, but had no effect on the glial-derived 
      neurotrophic factor. However, only BDNF remained at low levels after exercise 
      interruption. In addition, exercise training significantly reduced the 
      phosphorylation status of PLCgamma-1, but not CREB, in the spinal cord dorsal horn in 
      response to nerve injury. Finally, prolonged swim exercise reversed astrocyte and 
      microglia hyperactivity in the dorsal horn after nerve lesion, which remained 
      normalized after training cessation. Together, these results demonstrate that 
      exercise therapy induces long-lasting analgesia through various mechanisms 
      associated with the onset and advanced stages of neuropathy. Moreover, the data 
      support further studies to clarify whether appropriate exercise intensity, 
      volume, and duration can also cause long-lasting pain relief in patients with 
      neuropathic pain.
FAU - Almeida, Cayo
AU  - Almeida C
AD  - Laboratory of Pain Neurobiology, Department of Physiology, Ribeirao Preto School 
      of Medicine, University of Sao Paulo, Brazil Department of Biochemistry and 
      Immunology, Ribeirao Preto School of Medicine, University of Sao Paulo, Brazil 
      Federal Institute of Education, Science and Technology of Goias, Brazil School of 
      Physical Education and Sport of Ribeirao Preto, University of Sao Paulo, Brazil.
FAU - DeMaman, Aline
AU  - DeMaman A
FAU - Kusuda, Ricardo
AU  - Kusuda R
FAU - Cadetti, Flaviane
AU  - Cadetti F
FAU - Ravanelli, Maria Ida
AU  - Ravanelli MI
FAU - Queiroz, Andre L
AU  - Queiroz AL
FAU - Sousa, Thais A
AU  - Sousa TA
FAU - Zanon, Sonia
AU  - Zanon S
FAU - Silveira, Leonardo R
AU  - Silveira LR
FAU - Lucas, Guilherme
AU  - Lucas G
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Pain
JT  - Pain
JID - 7508686
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Glial Fibrillary Acidic Protein)
RN  - EC 2.3.1.48 (CREB-Binding Protein)
RN  - EC 2.3.3.1 (Citrate (si)-Synthase)
RN  - EC 3.1.4.3 (Phospholipase C gamma)
SB  - IM
MH  - Adaptation, Physiological
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - CREB-Binding Protein/metabolism
MH  - Citrate (si)-Synthase
MH  - Disease Models, Animal
MH  - Exercise Therapy/*methods
MH  - Glial Fibrillary Acidic Protein/metabolism
MH  - Heart/physiopathology
MH  - Hyperalgesia/etiology
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Muscle, Skeletal/physiopathology
MH  - Neuralgia/complications/pathology/*rehabilitation
MH  - Neuroglia/*metabolism/pathology
MH  - Pain Measurement
MH  - Pain Threshold/physiology
MH  - Phospholipase C gamma/metabolism
MH  - Phosphorylation
MH  - Time Factors
MH  - Up-Regulation/*physiology
EDAT- 2015/02/18 06:00
MHDA- 2015/11/03 06:00
CRDT- 2015/02/18 06:00
PHST- 2015/02/18 06:00 [entrez]
PHST- 2015/02/18 06:00 [pubmed]
PHST- 2015/11/03 06:00 [medline]
AID - 00006396-201503000-00019 [pii]
AID - 10.1097/01.j.pain.0000460339.23976.12 [doi]
PST - ppublish
SO  - Pain. 2015 Mar;156(3):504-513. doi: 10.1097/01.j.pain.0000460339.23976.12.