在突触周围星形胶质细胞投射模型中,三磷酸肌醇扩散在纳米尺度上的数量级分析支持突触神经元-星形胶质细胞的通信。

Q1 Biochemistry, Genetics and Molecular Biology BMC Biophysics Pub Date : 2018-02-12 eCollection Date: 2018-01-01 DOI:10.1186/s13628-018-0043-3
Pavel Montes de Oca Balderas, Horacio Montes de Oca Balderas
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引用次数: 14

摘要

背景:几十年来,星形胶质细胞被认为只是大脑的支持细胞。然而,在星形胶质细胞结缔组织中观察到的Ca2+波、它们的神经递质受体表达和胶质递质分泌提示其在信息处理、受孕等方面的作用存在一些争议。由肌醇三磷酸(SN-AmcIP3)介导的突触神经元-星形胶质细胞代谢通讯得到了不同报道的支持。然而,一些模型与这一观点相矛盾,在突触周围星形胶质细胞突起(PAP)中,Ca2+储存距离突触后密度为1000±325 nm,表明SN-AmcIP3是突触外的。然而,这一假设没有考虑到IP3扩散系数(Dab),它可以激活IP3受体(IP3R)从细胞内释放Ca2+。结果:在这项工作中,我们理想化了PAP (PAPm)模型,使用瞬态质量扩散模型对IP3扩散进行了数量级分析。该模型表明,IP3沿着PAPm形成浓度梯度,在毫秒内达到稳态,比IP3降解早三个数量级。该模型预测,Ca2+库附近的IP3浓度可能激活IP3R,这取决于磷脂酶C (PLC)的数量和活性。此外,PAPm支持IP3和细胞外Ca2+进入协同促进全局Ca2+瞬态。结论:该模型表明Ca2+在PAP中的储存位置不限制SN-AmcIP3。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Synaptic neuron-astrocyte communication is supported by an order of magnitude analysis of inositol tris-phosphate diffusion at the nanoscale in a model of peri-synaptic astrocyte projection.

Background: Astrocytes were conceived for decades only as supporting cells of the brain. However, the observation of Ca2+ waves in astrocyte synctitia, their neurotransmitter receptor expression and gliotransmitter secretion suggested a role in information handling, conception that has some controversies. Synaptic Neuron-Astrocyte metabotropic communication mediated by Inositol tris-phosphate (SN-AmcIP3) is supported by different reports. However, some models contradict this idea and Ca2+ stores are 1000 ± 325 nm apart from the Postsynaptic Density in the Perisynaptic Astrocyte Projections (PAP's), suggesting that SN-AmcIP3 is extrasynaptic. However, this assumption does not consider IP3 Diffusion Coefficient (Dab), that activates IP3 Receptor (IP3R) releasing Ca2+ from intracellular stores.

Results: In this work we idealized a model of a PAP (PAPm) to perform an order of magnitude analysis of IP3 diffusion using a transient mass diffusion model. This model shows that IP3 forms a concentration gradient along the PAPm that reaches the steady state in milliseconds, three orders of magnitude before IP3 degradation. The model predicts that IP3 concentration near the Ca2+ stores may activate IP3R, depending upon Phospholipase C (PLC) number and activity. Moreover, the PAPm supports that IP3 and extracellular Ca2+ entry synergize to promote global Ca2+ transients.

Conclusion: The model presented here indicates that Ca2+ stores position in PAP's does not limit SN-AmcIP3.

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BMC Biophysics
BMC Biophysics BIOPHYSICS-
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