树突中 Na1.2 依赖性逆行动作电位的丧失导致自闭症和智力障碍。
Loss of Na1.2-Dependent Backpropagating Action Potentials in Dendrites Contributes to Autism and Intellectual Disability.
机构信息
Department of Pharmacology, Yale University School of Medicine, New Haven, CT 06520, USA; Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06520, USA.
出版信息
Neuron. 2019 Aug 21;103(4):551-553. doi: 10.1016/j.neuron.2019.07.032.
PMID:31437449
Abstract
Mutations in voltage-dependent sodium channels cause severe autism/intellectual disability. In this issue of Neuron, Spratt et al. (2019) show that lowering expression of Nav1.2 channels attenuates backpropagation of action potentials into dendrites of cortical neurons, preventing spike-timing-dependent synaptic plasticity.
摘要
电压门控钠离子通道的突变可导致严重自闭症/智力障碍。在本期《神经元》杂志上，Spratt 等人（2019）表明，降低 Nav1.2 通道的表达可减弱动作电位逆行传入皮质神经元树突，从而阻止了依赖于发放时间的突触可塑性。
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