PMID- 30986502
OWN - NLM
STAT- MEDLINE
DCOM- 20200424
LR  - 20200424
IS  - 1872-9754 (Electronic)
IS  - 0197-0186 (Linking)
VI  - 128
DP  - 2019 Sep
TI  - Role of the BDNF-TrkB pathway in KCC2 regulation and rehabilitation following 
      neuronal injury: A mini review.
PG  - 32-38
LID - S0197-0186(18)30666-1 [pii]
LID - 10.1016/j.neuint.2019.04.003 [doi]
AB  - In most mature neurons, low levels of intracellular Cl(-) concentrations 
      ([Cl(-)](i)) are maintained by channels and transporters, particularly the 
      K(+)-Cl(-) cotransporter 2 (KCC2), which is the only Cl(-) extruder in most 
      neurons. Recent studies have implicated KCC2 expression in the molecular 
      mechanisms underlying neuronal disorders, such as spasticity, epilepsy and 
      neuropathic pain. Alterations in KCC2 expression have been associated with 
      brain-derived neurotrophic factor (BDNF) and its receptor tropomyosin-related 
      kinase B (TrkB). The present review summarizes recent progress regarding the 
      roles of Cl(-) regulators in immature and mature neurons. Moreover, we focus on 
      the role of KCC2 regulation via the BDNF-TrkB pathway in spinal cord injury and 
      rehabilitation, as prior studies have shown that the BDNF-TrkB pathway can affect 
      both the pathological development and functional amelioration of spinal cord 
      injuries. Evidence suggests that rehabilitation using active exercise and 
      mechanical stimulation can attenuate spasticity and neuropathic pain in animal 
      models, likely due to the upregulation of KCC2 expression via the BDNF-TrkB 
      pathway. Moreover, research suggests that such rehabilitation efforts may recover 
      KCC2 expression without the use of exogenous BDNF.
CI  - Copyright (c) 2019. Published by Elsevier Ltd.
FAU - Lee-Hotta, Sachiko
AU  - Lee-Hotta S
AD  - Department of Rehabilitation Sciences, Graduate School of Medicine, Nagoya 
      University, 1-1-20, Daiko-minami Higashi-ku, Nagoya-shi, Aichi, 461-8673, Japan. 
      Electronic address: lee@met.nagoya-u.ac.jp.
FAU - Uchiyama, Yasushi
AU  - Uchiyama Y
AD  - Department of Rehabilitation Sciences, Graduate School of Medicine, Nagoya 
      University, 1-1-20, Daiko-minami Higashi-ku, Nagoya-shi, Aichi, 461-8673, Japan. 
      Electronic address: uchiyama@met.nagoya-u.ac.jp.
FAU - Kametaka, Satoshi
AU  - Kametaka S
AD  - Department of Rehabilitation Sciences, Graduate School of Medicine, Nagoya 
      University, 1-1-20, Daiko-minami Higashi-ku, Nagoya-shi, Aichi, 461-8673, Japan. 
      Electronic address: kametaks@met.nagoya-u.ac.jp.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20190412
PL  - England
TA  - Neurochem Int
JT  - Neurochemistry international
JID - 8006959
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (SLC12A5 protein, human)
RN  - 0 (Symporters)
RN  - 7171WSG8A2 (BDNF protein, human)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - EC 2.7.10.1 (tropomyosin-related kinase-B, human)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*physiology
MH  - Membrane Glycoproteins/*physiology
MH  - Nervous System Diseases/*metabolism/*rehabilitation
MH  - Neurological Rehabilitation/*trends
MH  - Receptor, trkB/*physiology
MH  - Signal Transduction/physiology
MH  - Symporters/*physiology
OTO - NOTNLM
OT  - BDNF-TrkB pathway
OT  - KCC2
OT  - Spasticity
OT  - Spinal cord injury
EDAT- 2019/04/16 06:00
MHDA- 2020/04/25 06:00
CRDT- 2019/04/16 06:00
PHST- 2018/11/30 00:00 [received]
PHST- 2019/03/04 00:00 [revised]
PHST- 2019/04/08 00:00 [accepted]
PHST- 2019/04/16 06:00 [pubmed]
PHST- 2020/04/25 06:00 [medline]
PHST- 2019/04/16 06:00 [entrez]
AID - S0197-0186(18)30666-1 [pii]
AID - 10.1016/j.neuint.2019.04.003 [doi]
PST - ppublish
SO  - Neurochem Int. 2019 Sep;128:32-38. doi: 10.1016/j.neuint.2019.04.003. Epub 2019 
      Apr 12.