Rapid Homeostatic Plasticity of Intrinsic Excitability in a Central Pattern Generator Network Stabilizes Functional Neural Network Output
Rapid Homeostatic Plasticity of Intrinsic Excitability in a Central Pattern Generator Network Stabilizes Functional Neural Network Output
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DOI：
10.1523/jneurosci.1945-12.2012
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发表时间：
2012-07-11
影响因子：
5.3
通讯作者：
Schulz, David J.
中科院分区：
文献类型：
--
作者：
Ransdell, Joseph L.;Nair, Satish S.;Schulz, David J.
神经元和网络经历一个稳态可塑性的过程，通过将活动水平与网络和细胞特性相结合来稳定输出，以对抗长期扰动。在这里，我们描述了一对钾电流，I-A和I-KCa，稳定的内在兴奋性和网络功能的螃蟹，巨蟹座的心脏神经节之间的快速补偿相互作用。我们确定，在单个识别的神经元中编码I-A和I-KCa的通道的mRNA水平是正相关的，但在运动神经元群体中，离子电流本身是负相关的。然后，我们确定这些电流在功能上是耦合的;神经元内任何一种电流的水平降低都会导致另一种电流的快速增加。这种功能上的相互依赖导致个体神经元和网络输出的稳态稳定。此外，这些代偿性增加是机械独立的，这表明神经网络输出的维持对于生存至关重要。总之，我们生成了一个完整的模型，从mRNA到网络输出的稳态可塑性，其中快速的翻译后补偿机制作用于在基因表达水平上调节的通道蛋白质的储库，提供细胞和网络活动的稳态稳定。
Neurons and networks undergo a process of homeostatic plasticity that stabilizes output by integrating activity levels with network and cellular properties to counter longer-term perturbations. Here we describe a rapid compensatory interaction among a pair of potassium currents, I-A and I-KCa, that stabilizes both intrinsic excitability and network function in the cardiac ganglion of the crab, Cancer borealis. We determined that mRNA levels in single identified neurons for the channels which encode I-A and I-KCa are positively correlated, yet the ionic currents themselves are negatively correlated, across a population of motor neurons. We then determined that these currents are functionally coupled; decreasing levels of either current within a neuron causes a rapid increase in the other. This functional interdependence results in homeostatic stabilization of both the individual neuronal and the network output. Furthermore, these compensatory increases are mechanistically independent, suggesting robustness in the maintenance of neural network output that is critical for survival. Together, we generate a complete model for homeostatic plasticity from mRNA to network output where rapid post-translational compensatory mechanisms acting on a reservoir of channels proteins regulated at the level of gene expression provide homeostatic stabilization of both cellular and network activity.