Yang Xin, Bao Yifei, Xu Jindong, Gong Ru, Zhang Nan, Cai Lei, Xia Mingmei, Wang Jingjing, Lu Wei
State Key Laboratory of Bioelectronics, Key Laboratory of Developmental Genes and Human Disease, Ministry of Education, Institute of Life Sciences, Southeast University, Nanjing, Jiangsu Province 210096, China.
Co-innovation Center of Neuroregeneration, Nantong University, Nantong, Jiangsu Province 226001, People's Republic of China.
Cereb Cortex. 2020 Mar 14;30(3):1436-1446. doi: 10.1093/cercor/bhz177.
Integrated neural inputs from different dendrites converge at the soma for action potential generation. However, it is unclear how the convergent dendritic inputs interact at the soma and whether they can be further modified there. We report here an entirely new plasticity rule in hippocampal neurons in which repetitive pairing of subthreshold excitatory inputs from proximal apical and basal dendrites at a precise interval induces persistent bidirectional modifications of the two dendritic inputs. Strikingly, the modification of the dendritic inputs specially occurs at soma in the absence of somatic action potential and requires activation of somatic N-methyl-D-aspartate receptors (NMDARs). Once induced, the somatic modification can also be observed in other unpaired dendritic inputs upon their arrival at the soma. We further reveal that the soma can employ an active mechanism to potentiate the dendritic inputs by promoting sustained activation of somatic NMDARs and subsequent down-regulating of the fast inactivating A-type potassium current (IA) at the soma. Thus, the input-timing-dependent somatic plasticity we uncovered here is in sharp contrast to conventional forms of synaptic plasticity that occur at the dendrites and is important to somatic action potential generation.
来自不同树突的整合神经输入在胞体汇聚以产生动作电位。然而,尚不清楚汇聚的树突输入在胞体如何相互作用,以及它们在那里是否能被进一步修饰。我们在此报告海马神经元中一种全新的可塑性规则,即来自近端顶树突和基底树突的阈下兴奋性输入以精确间隔重复配对,可诱导这两种树突输入产生持续的双向修饰。引人注目的是,树突输入的修饰特别发生在没有胞体动作电位的胞体处,并且需要激活胞体 N - 甲基 - D - 天冬氨酸受体(NMDARs)。一旦诱导产生,在其他未配对的树突输入到达胞体时,也能观察到胞体修饰。我们进一步揭示,胞体可利用一种主动机制,通过促进胞体 NMDARs 的持续激活以及随后下调胞体处快速失活的 A 型钾电流(IA)来增强树突输入。因此,我们在此发现的依赖输入时间的胞体可塑性与发生在树突的传统形式的突触可塑性形成鲜明对比,并且对胞体动作电位的产生很重要。