Potassium Channels: A Potential Therapeutic Target for Parkinson's Disease.
10.1007/s12264-017-0177-3
- Author:
Xiaoyan CHEN
1
;
Bao XUE
1
;
Jun WANG
1
;
Haixia LIU
1
;
Limin SHI
2
;
Junxia XIE
3
Author Information
1. Collaborative Innovation Center for Brain Science, Department of Physiology, Shandong Provincial Collaborative Innovation Center for Neurodegenerative Disorders, Key Laboratory of Pathogenesis and Prevention of Neurological Disorders, Medical College of Qingdao University, Qingdao, 266071, China.
2. Collaborative Innovation Center for Brain Science, Department of Physiology, Shandong Provincial Collaborative Innovation Center for Neurodegenerative Disorders, Key Laboratory of Pathogenesis and Prevention of Neurological Disorders, Medical College of Qingdao University, Qingdao, 266071, China. slm0532@163.com.
3. Collaborative Innovation Center for Brain Science, Department of Physiology, Shandong Provincial Collaborative Innovation Center for Neurodegenerative Disorders, Key Laboratory of Pathogenesis and Prevention of Neurological Disorders, Medical College of Qingdao University, Qingdao, 266071, China. jxiaxie@public.qd.sd.cn.
- Publication Type:Journal Article
- Keywords:
A-type K+ channels;
Dopamine;
KV7/KCNQ channels;
Parkinson’s disease;
SK channels
- MeSH:
Animals;
Humans;
Parkinson Disease;
metabolism;
Potassium Channels;
metabolism
- From:Neuroscience Bulletin
2018;34(2):341-348
- CountryChina
- Language:English
-
Abstract:
The pathogenesis of the second major neurodegenerative disorder, Parkinson's disease (PD), is closely associated with the dysfunction of potassium (K) channels. Therefore, PD is also considered to be an ion channel disease or neuronal channelopathy. Mounting evidence has shown that K channels play crucial roles in the regulations of neurotransmitter release, neuronal excitability, and cell volume. Inhibition of K channels enhances the spontaneous firing frequency of nigral dopamine (DA) neurons, induces a transition from tonic firing to burst discharge, and promotes the release of DA in the striatum. Recently, three K channels have been identified to protect DA neurons and to improve the motor and non-motor symptoms in PD animal models: small conductance (SK) channels, A-type K channels, and K7/KCNQ channels. In this review, we summarize the physiological and pharmacological effects of the three K channels. We also describe in detail the laboratory investigations regarding K channels as a potential therapeutic target for PD.
