Endogenous rhythm generation in the pre-Bötzinger complex and ionic currents: modelling and in vitro studies.
Endogenous rhythm generation in the pre-Bötzinger complex and ionic currents: modelling and in vitro studies.
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前 Bötzinger 复合体和离子电流中的内源节律生成：建模和体外研究。
DOI：
10.1046/j.1460-9568.2003.02739.x
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发表时间：
2003
期刊：
影响因子：
--
通讯作者：
Pierrefiche,Olivier
中科院分区：
文献类型：
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作者：
Rybak,IlyaA;Shevtsova,NataliaA;St-John,WalterM;Paton,JulianFR;Pierrefiche,Olivier
前波青格复合体是哺乳动物脑干中参与呼吸节律产生的一个小区域。体外实验表明，该区域在一定条件下可产生内源性节律爆发活动。我们的调查集中在可能引起这种爆裂行为的条件。开发并分析了前Bötzinger复合体中起搏神经元群体的计算模型。每个神经元以Hodgkin-Huxley方式建模，包括持续性钠电流和延迟整流钾电流。我们发现，该模型的发射行为强烈依赖于这些电流的表达。具体而言，模型中的爆发可通过抑制延迟整流钾电流（直接或通过增加细胞外钾浓度[K+]o）或通过增强持续钠电流来诱导。为了测试我们的建模预测，我们记录了新生大鼠（P0-P4）的玻璃体脑干切片（700 µm）中前Bötzinger复合体的内源性群体活动和舌下神经（XII）的活动。 在3 mm[K+]时不存在节律性活动，但可通过[K+]升高至5-7 mm或应用钾电流阻断剂（4-AP，50-200 µm或TEA，2或4 mm）或通过NaCN（2 mm）阻断有氧代谢来触发。 这种节律性活动可以被持续性钠电流阻断剂利鲁唑（25或50 µm）消除。 这些发现在内源性爆发活动在体外呼吸节律产生和在体正常呼吸过程中的作用的背景下进行了讨论。vivovs.in喘着气
The pre‐Bötzinger complex is a small region in the mammalian brainstem involved in generation of the respiratory rhythm. As shownin vitro, this region, under certain conditions, can generate endogenous rhythmic bursting activity. Our investigation focused on the conditions that may induce this bursting behaviour. A computational model of a population of pacemaker neurons in the pre‐Bötzinger complex was developed and analysed. Each neuron was modelled in the Hodgkin–Huxley style and included persistent sodium and delayed‐rectifier potassium currents. We found that the firing behaviour of the model strongly depended on the expression of these currents. Specifically, bursting in the model could be induced by a suppression of delayed‐rectifier potassium current (either directly or via an increase in extracellular potassium concentration, [K+]o) or by an augmentation of persistent sodium current. To test our modelling predictions, we recorded endogenous population activity of the pre‐Bötzinger complex and activity of the hypoglossal (XII) nerve fromin vitrotransverse brainstem slices (700 µm) of neonatal rats (P0–P4). Rhythmic activity was absent at 3 mm[K+]obut could be triggered by either the elevation of [K+]oto 5–7 mmor application of potassium current blockers (4‐AP, 50–200 µm, or TEA, 2 or 4 mm), or by blocking aerobic metabolism with NaCN (2 mm). This rhythmic activity could be abolished by the persistent sodium current blocker riluzole (25 or 50 µm). These findings are discussed in the context of the role of endogenous bursting activity in the respiratory rhythm generationin vivovs.in vitroand during normal breathingin vivovs. gasping.