PMID- 32010056
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200928
IS  - 1664-2295 (Print)
IS  - 1664-2295 (Electronic)
IS  - 1664-2295 (Linking)
VI  - 10
DP  - 2019
TI  - Role of NKCC1 and KCC2 in Epilepsy: From Expression to Function.
PG  - 1407
LID - 10.3389/fneur.2019.01407 [doi]
LID - 1407
AB  - As a main inhibitory neurotransmitter in the central nervous system, 
      gamma-aminobutyric acid (GABA) activates chloride-permeable GABAa receptors (GABAa 
      Rs) and induces chloride ion (Cl(-)) flow, which relies on the intracellular 
      chloride concentration ([Cl(-)](i)) of the postsynaptic neuron. The Na-K-2Cl 
      cotransporter isoform 1 (NKCC1) and the K-Cl cotransporter isoform 2 (KCC2) are 
      two main cation-chloride cotransporters (CCCs) that have been implicated in human 
      epilepsy. NKCC1 and KCC2 reset [Cl(-)](i) by accumulating and extruding Cl(-), 
      respectively. Previous studies have shown that the profile of NKCC1 and KCC2 in 
      neonatal neurons may reappear in mature neurons under some pathophysiological 
      conditions, such as epilepsy. Although increasing studies focusing on the 
      expression of NKCC1 and KCC2 have suggested that impaired chloride plasticity may 
      be closely related to epilepsy, additional neuroelectrophysiological research 
      aimed at studying the functions of NKCC1 and KCC2 are needed to understand the 
      exact mechanism by which they induce epileptogenesis. In this review, we aim to 
      briefly summarize the current researches surrounding the expression and function 
      of NKCC1 and KCC2 in epileptogenesis and its implications on the treatment of 
      epilepsy. We will also explore the potential for NKCC1 and KCC2 to be therapeutic 
      targets for the development of novel antiepileptic drugs.
CI  - Copyright (c) 2020 Liu, Wang, Liang, Zhang and Yang.
FAU - Liu, Ru
AU  - Liu R
AD  - Neuroelectrophysiological Laboratory, Xuanwu Hospital, Capital Medical 
      University, Beijing, China.
AD  - Center of Epilepsy, Center for Brain Disorders Research, Capital Medical 
      University, Beijing, China.
AD  - Center of Epilepsy, Beijing Institute of Brain Disorders, Beijing, China.
AD  - Guangzhou Regenerative Medicine and Health Guangdong Laboratory, Guangzhou, 
      China.
FAU - Wang, Junling
AU  - Wang J
AD  - Neuroelectrophysiological Laboratory, Xuanwu Hospital, Capital Medical 
      University, Beijing, China.
AD  - Center of Epilepsy, Center for Brain Disorders Research, Capital Medical 
      University, Beijing, China.
AD  - Center of Epilepsy, Beijing Institute of Brain Disorders, Beijing, China.
AD  - Guangzhou Regenerative Medicine and Health Guangdong Laboratory, Guangzhou, 
      China.
FAU - Liang, Shuli
AU  - Liang S
AD  - Department of Functional Neurosurgery, Beijing Children's Hospital, Capital 
      Medical University, Beijing, China.
FAU - Zhang, Guojun
AU  - Zhang G
AD  - Department of Functional Neurosurgery, Xuanwu Hospital, Capital Medical 
      University, Beijing, China.
FAU - Yang, Xiaofeng
AU  - Yang X
AD  - Neuroelectrophysiological Laboratory, Xuanwu Hospital, Capital Medical 
      University, Beijing, China.
AD  - Center of Epilepsy, Center for Brain Disorders Research, Capital Medical 
      University, Beijing, China.
AD  - Center of Epilepsy, Beijing Institute of Brain Disorders, Beijing, China.
AD  - Guangzhou Regenerative Medicine and Health Guangdong Laboratory, Guangzhou, 
      China.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20200117
PL  - Switzerland
TA  - Front Neurol
JT  - Frontiers in neurology
JID - 101546899
PMC - PMC6978738
OTO - NOTNLM
OT  - KCC2
OT  - NKCC1
OT  - bumetanide
OT  - electrophysiology
OT  - epilepsy
EDAT- 2020/02/06 06:00
MHDA- 2020/02/06 06:01
PMCR- 2020/01/17
CRDT- 2020/02/04 06:00
PHST- 2019/04/11 00:00 [received]
PHST- 2019/12/23 00:00 [accepted]
PHST- 2020/02/04 06:00 [entrez]
PHST- 2020/02/06 06:00 [pubmed]
PHST- 2020/02/06 06:01 [medline]
PHST- 2020/01/17 00:00 [pmc-release]
AID - 10.3389/fneur.2019.01407 [doi]
PST - epublish
SO  - Front Neurol. 2020 Jan 17;10:1407. doi: 10.3389/fneur.2019.01407. eCollection 
      2019.