Kv3 CHANNELS: ENABLERS OF RAPID FIRING, NEUROTRANSMITTER RELEASE, AND NEURONAL ENDURANCE

被引:130
作者
Kaczmarek, Leonard K. [1 ]
Zhang, Yalan
机构
[1] Yale Univ, Sch Med, Dept Pharmacol, 333 Cedar St,POB 208066, New Haven, CT 06520 USA
基金
美国国家卫生研究院;
关键词
GATED POTASSIUM CHANNEL; AUDITORY BRAIN-STEM; RAT COCHLEAR NUCLEUS; ACTION-POTENTIAL REPOLARIZATION; CEREBELLAR PURKINJE-CELLS; CENTRAL-NERVOUS-SYSTEM; ATAXIA TYPE 13; INFERIOR COLLICULUS NEURONS; MENTAL-RETARDATION PROTEIN; FAST-SPIKING INTERNEURONS;
D O I
10.1152/physrev.00002.2017
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
The intrinsic electrical characteristics of different types of neurons are shaped by the K+ channels they express. From among the more than 70 different K+ channel genes expressed in neurons, Kv3 family voltage-dependent K+ channels are uniquely associated with the ability of certain neurons to fire action potentials and to release neurotransmitter at high rates of up to 1,000 Hz. In general, the four Kv3 channels Kv3.1-Kv3.4 share the property of activating and deactivating rapidly at potentials more positive than other channels. Each Kv3 channel gene can generate multiple protein isoforms, which contribute to the high-frequency firing of neurons such as auditory brain stem neurons, fast-spiking GABAergic interneurons, and Purkinje cells of the cerebellum, and to regulation of neurotransmitter release at the terminals of many neurons. The different Kv3 channels have unique expression patterns and biophysical properties and are regulated in different ways by protein kinases. In this review, we cover the function, localization, and modulation of Kv3 channels and describe how levels and properties of the channels are altered by changes in ongoing neuronal activity. We also cover how the protein-protein interaction of these channels with other proteins affects neuronal functions, and how mutations or abnormal regulation of Kv3 channels are associated with neurological disorders such as ataxias, epilepsies, schizophrenia, and Alzheimer's disease.
引用
收藏
页码:1431 / 1468
页数:38
相关论文
共 265 条
[101]   BIOPHYSICAL AND MOLECULAR MECHANISMS OF SHAKER POTASSIUM CHANNEL INACTIVATION [J].
HOSHI, T ;
ZAGOTTA, WN ;
ALDRICH, RW .
SCIENCE, 1990, 250 (4980) :533-538
[102]   Coexpression of high-voltage-activated ion channels Kv3.4 and Cav1.2 in pioneer axons during pathfinding in the developing rat forebrain [J].
Huang, Chia-Yi ;
Chu, Dachen ;
Hwang, Wei-Chao ;
Tsaur, Meei-Ling .
JOURNAL OF COMPARATIVE NEUROLOGY, 2012, 520 (16) :3650-3672
[103]   Purkinje-cell-restricted restoration of Kv3.3 function restores complex spikes and rescues motor coordination in Kcnc3 mutants [J].
Hurlock, Edward C. ;
McMahon, Anne ;
Joho, Rolf H. .
JOURNAL OF NEUROSCIENCE, 2008, 28 (18) :4640-4648
[104]   Rescue of Motor Coordination by Purkinje Cell-Targeted Restoration of Kv3.3 Channels in Kcnc3-Null Mice Requires Kcnc1 [J].
Hurlock, Edward C. ;
Bose, Mitali ;
Pierce, Ganon ;
Joho, Rolf H. .
JOURNAL OF NEUROSCIENCE, 2009, 29 (50) :15735-15744
[105]   Fast regulation of axonal growth cone motility by electrical activity [J].
Ibarretxe, Gaskon ;
Perrais, David ;
Jaskolski, Frederic ;
Vimeney, Alice ;
Mulle, Christophe .
JOURNAL OF NEUROSCIENCE, 2007, 27 (29) :7684-7695
[106]   A voltage-gated potassium channel, Kv3.1b, is expressed by a subpopulation of large pyramidal neurons in layer 5 of the macaque monkey cortex [J].
Ichinohe, N ;
Watakabe, A ;
Miyashita, T ;
Yamamori, T ;
Hashikawa, T ;
Rockland, KS .
NEUROSCIENCE, 2004, 129 (01) :179-185
[107]   Kv3.3 channels harbouring a mutation of spinocerebellar ataxia type 13 alter excitability and induce cell death in cultured cerebellar Purkinje cells [J].
Irie, Tomohiko ;
Matsuzaki, Yasunori ;
Sekino, Yuko ;
Hirai, Hirokazu .
JOURNAL OF PHYSIOLOGY-LONDON, 2014, 592 (01) :229-247
[108]   Neurodevelopmental abnormalities associated with severe congenital neutropenia due to the R86X mutation in the HAX1 gene [J].
Ishikawa, N. ;
Okada, S. ;
Miki, M. ;
Shirao, K. ;
Kihara, H. ;
Tsumura, M. ;
Nakamura, K. ;
Kawaguchi, H. ;
Ohtsubo, M. ;
Yasunaga, S. ;
Matsubara, K. ;
Sako, M. ;
Hara, J. ;
Shiohara, M. ;
Kojima, S. ;
Sato, T. ;
Takihara, Y. ;
Kobayashi, M. .
JOURNAL OF MEDICAL GENETICS, 2008, 45 (12) :802-807
[109]  
Ishikawa T, 2003, J NEUROSCI, V23, P10445
[110]   Spinocerebellar ataxia type 13 mutation that is associated with disease onset in infancy disrupts axonal pathfinding during neuronal development [J].
Issa, Fadi A. ;
Mock, Allan F. ;
Sagasti, Alvaro ;
Papazian, Diane M. .
DISEASE MODELS & MECHANISMS, 2012, 5 (06) :921-929