Respiratory pattern generator model using Ca++-induced Ca++ release in neurons shows both pacemaker and reciprocal network properties.
Respiratory pattern generator model using Ca++-induced Ca++ release in neurons shows both pacemaker and reciprocal network properties.
复制标题
使用 Ca 诱导神经元中 Ca 释放的呼吸模式生成器模型显示了起搏器和互惠网络特性。
DOI：
10.1007/s00422-003-0418-6
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发表时间：
2003
期刊：
影响因子：
--
通讯作者：
Orem,JM
中科院分区：
文献类型：
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作者：
Dunin-Barkowski,WL;Escobar,AL;Lovering,AT;Orem,JM
对于中枢呼吸节律发生有两种相互矛盾的解释。有人认为，呼吸节律是由吸气和呼气神经半中心之间的相互作用产生的，它们相互抑制，从而提供相互的节律活动（Brown 1914）。另一种是利用单个神经元的突发起搏器活动来产生节律（Feldman 和 Cleland 1982）。人们开发了混合模型来协调这两种看似冲突的机制（Smith 等人，2000 年；Rybak 等人，2001 年）。在这里，我们报告了计算机模拟，演示了两种类型振荡器的统一机制。在模型中，我们使用 Ca++ 依赖性 K+ 通道（Mifflin 等人，1985）与 Ca++ 诱导的细胞内储存的 Ca++ 释放（McPherson 和 Campbell，1993）之间的相互作用，最近在神经元中发现了这种相互作用（Hernandez-Cruz 等人，1997 年；Mitra 和 Slaughter 2002a,b；Scornik 等人，2001 年）。我们的计算表明，当暴露于稳定的兴奋性输入时，具有这些细胞内机制的未耦合神经元表现出条件起搏器特性（Butera 等人，1999）。在两个模型神经池之间添加弱抑制性突触（基于增加的 K+ 电导率）令人惊讶地同步了两个神经池的活动。随着两个池之间的抑制性突触连接从零增加到更高的值，该模型首先产生单个神经元的分离起搏器活动，然后产生所有神经元（吸气和呼气）的周期性同步爆发，最后产生神经池的相互节律活动。
There are two contradictory explanations for central respiratory rhythmogenesis. One suggests that respiratory rhythm emerges from interaction between inspiratory and expiratory neural semicenters that inhibit each other and thereby provide reciprocal rhythmic activity (Brown 1914). The other uses bursting pacemaker activity of individual neurons to produce the rhythm (Feldman and Cleland 1982). Hybrid models have been developed to reconcile these two seemingly conflicting mechanisms (Smith et al. 2000; Rybak et al. 2001). Here we report computer simulations that demonstrate a unified mechanism of the two types of oscillator. In the model, we use the interaction of Ca++-dependent K+channels (Mifflin et al. 1985) with Ca++-induced Ca++release from intracellular stores (McPherson and Campbell 1993), which was recently revealed in neurons (Hernandez-Cruz et al. 1997; Mitra and Slaughter 2002a,b; Scornik et al. 2001). Our computations demonstrate that uncoupled neurons with these intracellular mechanisms show conditional pacemaker properties (Butera et al. 1999) when exposed to steady excitatory inputs. Adding weak inhibitory synapses (based on increased K+conductivity) between two model neural pools surprisingly synchronizes the activity of both neural pools. As inhibitory synaptic connections between the two pools increase from zero to higher values, the model produces first dissociated pacemaker activity of individual neurons, then periodic synchronous bursts of all neurons (inspiratory and expiratory), and finally reciprocal rhythmic activity of the neural pools.