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首页> 美国卫生研究院文献>Frontiers in Computational Neuroscience >The Effects of Medium Spiny Neuron Morphologcial Changes on Basal Ganglia Network under External Electric Field: A Computational Modeling Study
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The Effects of Medium Spiny Neuron Morphologcial Changes on Basal Ganglia Network under External Electric Field: A Computational Modeling Study

机译：外电场作用下基底神经节网络中棘状神经元形态变化的影响：计算模型研究

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The damage of dopaminergic neurons that innervate the striatum has been considered to be the proximate cause of Parkinson's disease (PD). In the dopamine-denervated state, the loss of dendritic spines and the decrease of dendritic length may prevent medium spiny neuron (MSN) from receiving too much excitatory stimuli from the cortex, thereby reducing the symptom of Parkinson's disease. However, the reduction in dendritic spine density obtained by different experiments is significantly different. We developed a biological-based network computational model to quantify the effect of dendritic spine loss and dendrites tree degeneration on basal ganglia (BG) signal regulation. Through the introduction of error index (EI), which was used to measure the attenuation of the signal, we explored the amount of dendritic spine loss and dendritic trees degradation required to restore the normal regulatory function of the network, and found that there were two ranges of dendritic spine loss that could reduce EI to normal levels in the case of dopamine at a certain level, this was also true for dendritic trees. However, although these effects were the same, the mechanisms of these two cases were significant difference. Using the method of phase diagram analysis, we gained insight into the mechanism of signal degradation. Furthermore, we explored the role of cortex in MSN morphology changes dopamine depletion-induced and found that proper adjustments to cortical activity do stop the loss in dendritic spines induced by dopamine depleted. These results suggested that modifying cortical drive onto MSN might provide a new idea on clinical therapeutic strategies for Parkinson's disease.
机译：支配纹状体的多巴胺能神经元的损害被认为是帕金森氏病（PD）的近因。在多巴胺去神经状态下，树突棘的丧失和树突长度的减少可能阻止中棘神经元（MSN）从皮质接受过多的兴奋性刺激，从而减轻帕金森氏病的症状。但是，通过不同的实验获得的树突状脊柱密度的降低是明显不同的。我们开发了一种基于生物学的网络计算模型，以量化树突状脊柱丢失和树突状树变性对基底神经节（BG）信号调节的影响。通过引入用于测量信号衰减的错误指数（EI），我们探索了恢复网络正常调节功能所需的树突棘损失和树突树退化的数量，发现其中有两个在多巴胺达到一定水平的情况下，可以将EI降至正常水平的树突棘损失范围，对于树突树也是如此。然而，尽管这些效果是相同的，但这两个案例的机制却存在显着差异。使用相图分析方法，我们了解了信号衰减的机理。此外，我们探讨了皮质在多巴胺耗竭诱导的MSN形态变化中的作用，并发现对皮质活性的适当调整确实阻止了由多巴胺耗竭引起的树突棘的损失。这些结果表明，修改皮层驱动到MSN上可能为帕金森氏病的临床治疗策略提供新思路。

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