钠离子泄漏通道与神经元兴奋性和节律性行为。
Sodium leak channels in neuronal excitability and rhythmic behaviors.
机构信息
Department of Biology, University of Pennsylvania, Philadelphia, PA 19104, USA.
出版信息
Neuron. 2011 Dec 22;72(6):899-911. doi: 10.1016/j.neuron.2011.12.007.
Abstract
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.
摘要
细胞外的 K⁺、Na⁺和 Ca²⁺离子都会影响神经元的静息膜电位。然而，细胞外的 Na⁺和 Ca²⁺调节基础神经元兴奋性的机制还不是很清楚。最近的研究结果表明，NALCN 与 UNC79 和 UNC80 一起，为神经元提供基础的 Na⁺渗漏电导。Nalcn、Unc79 或 Unc80 的突变会导致严重的表型，包括新生儿致死和节律行为紊乱。本综述讨论了 NALCN 复合物的特性、调节及其对神经元功能和动物行为的贡献。
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