Sodium Leak Channels in Neuronal Excitability and Rhythmic Behaviors

被引：112
作者：
Ren, Dejian [1 ]
机构：
[1] Univ Penn, Dept Biol, Philadelphia, PA 19104 USA
来源：
NEURON | 2011年 / 72卷 / 06期
关键词：
VOLTAGE-GATED SODIUM; CALCIUM-SENSING RECEPTOR; EXTRACELLULAR CALCIUM; CATION CHANNEL; ION-CHANNEL; SUBSTANCE-P; SYNAPTIC-TRANSMISSION; EPILEPTIFORM ACTIVITY; MOLECULAR-CLONING; K+ CHANNEL;
D O I：
10.1016/j.neuron.2011.12.007
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
Extracellular K, Na+, and Ca2+ ions all influence the resting membrane potential of the neuron. However, the mechanisms by which extracellular Na+ and Ca2+ regulate basal neuronal excitability are not well understood. Recent findings suggest that NALCN, in association with UNC79 and UNC80, contributes a basal Na+ leak conductance in neurons. Mutations in Nalcn, Unc79, or Unc80 lead to severe phenotypes that include neonatal lethality and disruption in rhythmic behaviors. This review discusses the properties of the NALCN complex, its regulation, and its contribution to neuronal function and animal behavior.
引用
收藏
页码：899 / 911
页数：13
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