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产生呼吸节律量子减慢的呼吸神经网络双振荡器模型。

Dual oscillator model of the respiratory neuronal network generating quantal slowing of respiratory rhythm.

作者信息

Lal Amit, Oku Yoshitaka, Hülsmann Swen, Okada Yasumasa, Miwakeichi Fumikazu, Kawai Shigeharu, Tamura Yoshiyasu, Ishiguro Makio

机构信息

Department of Physiology, Hyogo College of Medicine, Nishinomiya, Hyogo, 663-8501, Japan.

出版信息

J Comput Neurosci. 2011 Apr;30(2):225-40. doi: 10.1007/s10827-010-0249-0. Epub 2010 Jun 11.

Abstract

We developed a dual oscillator model to facilitate the understanding of dynamic interactions between the parafacial respiratory group (pFRG) and the preBötzinger complex (preBötC) neurons in the respiratory rhythm generation. Both neuronal groups were modeled as groups of 81 interconnected pacemaker neurons; the bursting cell model described by Butera and others [model 1 in Butera et al. (J Neurophysiol 81:382-397, 1999a)] were used to model the pacemaker neurons. We assumed (1) both pFRG and preBötC networks are rhythm generators, (2) preBötC receives excitatory inputs from pFRG, and pFRG receives inhibitory inputs from preBötC, and (3) persistent Na(+) current conductance and synaptic current conductances are randomly distributed within each population. Our model could reproduce 1:1 coupling of bursting rhythms between pFRG and preBötC with the characteristic biphasic firing pattern of pFRG neurons, i.e., firings during pre-inspiratory and post-inspiratory phases. Compatible with experimental results, the model predicted the changes in firing pattern of pFRG neurons from biphasic expiratory to monophasic inspiratory, synchronous with preBötC neurons. Quantal slowing, a phenomena of prolonged respiratory period that jumps non-deterministically to integer multiples of the control period, was observed when the excitability of preBötC network decreased while strengths of synaptic connections between the two groups remained unchanged, suggesting that, in contrast to the earlier suggestions (Mellen et al., Neuron 37:821-826, 2003; Wittmeier et al., Proc Natl Acad Sci USA 105(46):18000-18005, 2008), quantal slowing could occur without suppressed or stochastic excitatory synaptic transmission. With a reduced excitability of preBötC network, the breakdown of synchronous bursting of preBötC neurons was predicted by simulation. We suggest that quantal slowing could result from a breakdown of synchronized bursting within the preBötC.

摘要

我们开发了一种双振荡器模型,以促进对呼吸节律产生过程中面神经旁呼吸组(pFRG)和前包钦格复合体(preBötC)神经元之间动态相互作用的理解。这两个神经元群体均被建模为81个相互连接的起搏器神经元组;采用Butera等人描述的爆发式细胞模型[Butera等人(《神经生理学杂志》81:382 - 397, 1999a)中的模型1]来模拟起搏器神经元。我们假设:(1)pFRG和preBötC网络都是节律发生器;(2)preBötC接受来自pFRG的兴奋性输入,而pFRG接受来自preBötC的抑制性输入;(3)持续性钠电流电导和突触电流电导在每个群体中随机分布。我们的模型能够重现pFRG和preBötC之间爆发节律的1:1耦合,并具有pFRG神经元典型的双相放电模式,即在吸气前和吸气后阶段放电。与实验结果一致,该模型预测pFRG神经元的放电模式从双相呼气转变为单相吸气,与preBötC神经元同步。当preBötC网络的兴奋性降低而两组之间突触连接强度保持不变时,观察到了量子减慢现象,即呼吸周期延长并随机跃升至控制周期的整数倍,这表明,与早期观点(Mellen等人,《神经元》37:821 - 826, 2003;Wittmeier等人,《美国国家科学院院刊》105(46):18000 - 18005, 2008)相反,量子减慢可能在没有抑制性或随机兴奋性突触传递受抑制的情况下发生。通过模拟预测,随着preBötC网络兴奋性降低,preBötC神经元同步爆发会瓦解。我们认为量子减慢可能是由于preBötC内同步爆发的瓦解所致。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57ab/3058346/c7e611912e18/10827_2010_249_Fig1_HTML.jpg

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