Burke Kenneth J, Bender Kevin J
Neuroscience Graduate Program and Department of Neurology, Kavli Institute for Fundamental Neuroscience, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, United States.
Front Cell Neurosci. 2019 May 17;13:221. doi: 10.3389/fncel.2019.00221. eCollection 2019.
The axon is responsible for integrating synaptic signals, generating action potentials (APs), propagating those APs to downstream synapses and converting them into patterns of neurotransmitter vesicle release. This process is mediated by a rich assortment of voltage-gated ion channels whose function can be affected on short and long time scales by activity. Moreover, neuromodulators control the activity of these proteins through G-protein coupled receptor signaling cascades. Here, we review cellular mechanisms and signaling pathways involved in axonal ion channel modulation and examine how changes to ion channel function affect AP initiation, AP propagation, and the release of neurotransmitter. We then examine how these mechanisms could modulate synaptic function by focusing on three key features of synaptic information transmission: synaptic strength, synaptic variability, and short-term plasticity. Viewing these cellular mechanisms of neuromodulation from a functional perspective may assist in extending these findings to theories of neural circuit function and its neuromodulation.
轴突负责整合突触信号，产生动作电位（APs），将这些动作电位传导至下游突触，并将其转化为神经递质囊泡释放模式。这一过程由丰富多样的电压门控离子通道介导，其功能可在短期和长期时间尺度上受活动影响。此外，神经调质通过G蛋白偶联受体信号级联反应控制这些蛋白质的活性。在此，我们综述轴突离子通道调节所涉及的细胞机制和信号通路，并研究离子通道功能的变化如何影响动作电位的起始、动作电位的传导以及神经递质的释放。然后，我们通过关注突触信息传递的三个关键特征：突触强度、突触变异性和短期可塑性，来研究这些机制如何调节突触功能。从功能角度审视这些神经调节的细胞机制，可能有助于将这些发现扩展到神经回路功能及其神经调节的理论中。
