Städele Carola, Stein Wolfgang
Institute of Neurobiology, Ulm University, 89069 Ulm, Germany, and School of Biological Sciences, Illinois State University, Normal, Illinois 61790.
School of Biological Sciences, Illinois State University, Normal, Illinois 61790
J Neurosci. 2016 Jun 22;36(25):6718-31. doi: 10.1523/JNEUROSCI.2753-15.2016.
Essential to understanding the process of neuronal signal integration is the knowledge of where within a neuron action potentials (APs) are generated. Recent studies support the idea that the precise location where APs are initiated and the properties of spike initiation zones define the cell's information processing capabilities. Notably, the location of spike initiation can be modified homeostatically within neurons to adjust neuronal activity. Here we show that this potential mechanism for neuronal plasticity can also be exploited in a rapid and dynamic fashion. We tested whether dislocation of the spike initiation zone affects signal integration by studying ectopic spike initiation in the anterior gastric receptor neuron (AGR) of the stomatogastric nervous system of Cancer borealis Like many other vertebrate and invertebrate neurons, AGR can generate ectopic APs in regions distinct from the axon initial segment. Using voltage-sensitive dyes and electrophysiology, we determined that AGR's ectopic spike activity was consistently initiated in the neuropil region of the stomatogastric ganglion motor circuits. At least one neurite branched off the AGR axon in this area; and indeed, we found that AGR's ectopic spike activity was influenced by local motor neurons. This sensorimotor interaction was state-dependent in that focal axon modulation with the biogenic amine octopamine, abolished signal integration at the primary spike initiation zone by dislocating spike initiation to a distant region of the axon. We demonstrate that the site of ectopic spike initiation is important for signal integration and that axonal neuromodulation allows for a dynamic adjustment of signal integration.
Although it is known that action potentials are initiated at specific sites in the axon, it remains to be determined how the precise location of action potential initiation affects neuronal activity and signal integration. We addressed this issue by studying ectopic spiking in the axon of a single-cell sensory neuron in the stomatogastric nervous system. Action potentials were consistently initiated at a specific region of the axon trunk, near a motor neuropil. Spike frequency was regulated by motor neuron activity, but only if spike initiation occurred at this location. Neuromodulation of the axon dislocated the site of initiation, resulting in abolishment of signal integration from motor neurons. Thus, neuromodulation allows for a dynamic adjustment of axonal signal integration.
理解神经元信号整合过程的关键在于了解神经元内动作电位（APs）产生的位置。最近的研究支持这样一种观点，即动作电位起始的精确位置以及峰电位起始区的特性决定了细胞的信息处理能力。值得注意的是，峰电位起始的位置可以在神经元内通过稳态调节进行改变，以调整神经元活动。在这里，我们表明这种神经元可塑性的潜在机制也可以以快速和动态的方式被利用。我们通过研究北方黄道蟹口胃神经系统前胃受体神经元（AGR）中的异位峰电位起始，来测试峰电位起始区的移位是否会影响信号整合。与许多其他脊椎动物和无脊椎动物神经元一样，AGR可以在与轴突起始段不同的区域产生异位动作电位。使用电压敏感染料和电生理学方法，我们确定AGR的异位峰电位活动始终在口胃神经节运动回路的神经毡区域起始。在这个区域至少有一条神经突从AGR轴突分支出来；事实上，我们发现AGR的异位峰电位活动受到局部运动神经元的影响。这种感觉运动相互作用是状态依赖的，因为用生物胺章鱼胺进行局部轴突调制，通过将峰电位起始移位到轴突的远处区域，消除了初级峰电位起始区的信号整合。我们证明异位峰电位起始的位置对信号整合很重要，并且轴突神经调制允许对信号整合进行动态调整。
虽然已知动作电位在轴突的特定部位起始，但动作电位起始的精确位置如何影响神经元活动和信号整合仍有待确定。我们通过研究口胃神经系统中单个细胞感觉神经元轴突中的异位放电来解决这个问题。动作电位始终在轴突主干的特定区域、靠近运动神经毡处起始。峰频率受运动神经元活动调节，但前提是峰电位起始发生在这个位置。轴突的神经调制使起始位置移位，导致来自运动神经元的信号整合被消除。因此，神经调制允许对轴突信号整合进行动态调整。
