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一种新颖的轴突断端(axon bleb)膜片钳记录方法大力促进了中枢神经系统轴突功能的研究。我们的工作应用这一方法揭示了大脑皮层锥体神经元的数码信号(具全或无特性的动作电位)的爆发和传播机制。在轴突始段(axon initial segment,AIS)远端高密度聚集的低阈值Na+通道亚型Nav1.6决定动作电位的爆发;而在AIS近端高密度聚集的高阈值Na+通道亚型Nav1.2促进动作电位向胞体和树突的反向传播。应用胞体和轴突的同时记录,我们发现胞体阈下膜电位的变化可以在轴突上传播较长的距离并可到达那些离胞体较近的突触前终末。进一步的研究证明了胞体膜电位的变化调控动作电位触发的突触传递,该膜电位依赖的突触传递是一种模拟式的信号传递。轴突上一类特殊K+通道(Kv1)的活动调制动作电位的波形,特别是其波宽,从而调控各种突触前膜电位水平下突触强度的变化。突触前终末的背景Ca2+浓度也可能参与模拟信号的传递。这些发现深化了我们对中枢神经系统内神经信号处理基本原理的认识,进而帮助我们理解脑如何工作。
A Novel Axon Bleb Patch-Clamp Recording Method Vigorously Promotes Axonal Function in the Central Nervous System. Our work applies this method to reveal the mechanism of burst and transmission of digital signals (with or without characteristic action potentials) in pyramidal neurons of the cerebral cortex. The low threshold Na + channel subtype Nav1.6 aggregated at a high density distal to the axon initial segment (AIS) determines the onset of action potentials; whereas the high threshold Na + channel subtype Nav1 aggregates at a high density in the proximal AIS. 2 to promote the action potential to the soma and dendrites reverse transmission. Using simultaneous recordings of soma and axons, we found that changes in subthreshold submucosal potentials can propagate longer distances on the axons and reach pre-synaptic terminals that are more proximal to the body. Further studies demonstrated that changes in cell membrane potential regulate the action potential-triggered synaptic transmission, which is an analogous signaling. The waveform of the action modulation action potential of a particular type of K + channel (Kv1) on the axon, in particular its wave width, regulates the change in synaptic intensity at various presynaptic membrane potential levels. The background Ca2 + concentration at presynaptic terminals may also be involved in the transmission of analog signals. These findings reinforce our understanding of the fundamentals of neural signal processing in the central nervous system and help us understand how the brain works.