4.5 Article

Reaction-Diffusion Model-Based Research on Formation Mechanism of Neuron Dendritic Spine Patterns

期刊

FRONTIERS IN NEUROROBOTICS
卷 15, 期 -, 页码 -

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fnbot.2021.563682

关键词

dendritic spine; Turing instability; reaction-diffusion model; branching morphogenesis; glioma

资金

  1. National Natural Science Foundation of China [62027812, U1813210, 61903201]
  2. Opening Foundation of Beijing Advanced Innovation Center for Intelligent Robots [2019IRS05]

向作者/读者索取更多资源

This study provided a reinterpretation of the relationship between dendritic spine pattern abnormalities and multiple nervous system diseases, and used a reaction-diffusion model to simulate the formation process of dendritic spines, investigating the factors affecting spine patterns. The research found that the consumption rate of substrates by the cytoskeleton, as well as the amount of an exogenous activator and inhibitor, are key factors in regulating spine shape and density. The study also analyzed the inner mechanism of how these factors regulate the dendritic spine pattern through Turing instability analysis, providing insights for potential treatment research for diseases related to dendritic spine pattern abnormalities.
The pattern abnormalities of dendritic spine, tiny protrusions on neuron dendrites, have been found related to multiple nervous system diseases, such as Parkinson's disease and schizophrenia. The determination of the factors affecting spine patterns is of vital importance to explore the pathogenesis of these diseases, and further, search the treatment method for them. Although the study of dendritic spines is a hot topic in neuroscience in recent years, there is still a lack of systematic study on the formation mechanism of its pattern. This paper provided a reinterpretation of reaction-diffusion model to simulate the formation process of dendritic spine, and further, study the factors affecting spine patterns. First, all four classic shapes of spines, mushroom-type, stubby-type, thin-type, and branched-type were reproduced using the model. We found that the consumption rate of substrates by the cytoskeleton is a key factor to regulate spine shape. Moreover, we found that the density of spines can be regulated by the amount of an exogenous activator and inhibitor, which is in accordance with the anatomical results found in hippocampal CA1 in SD rats with glioma. Further, we analyzed the inner mechanism of the above model parameters regulating the dendritic spine pattern through Turing instability analysis and drew a conclusion that an exogenous inhibitor and activator changes Turing wavelength through which to regulate spine densities. Finally, we discussed the deep regulation mechanisms of several reported regulators of dendritic spine shape and densities based on our simulation results. Our work might evoke attention to the mathematic model-based pathogenesis research for neuron diseases which are related to the dendritic spine pattern abnormalities and spark inspiration in the treatment research for these diseases.

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