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首页> 外文期刊>The European Journal of Neuroscience >Endogenous rhythm generation in the pre-Botzinger complex and ionic currents: modelling and in vitro studies.
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Endogenous rhythm generation in the pre-Botzinger complex and ionic currents: modelling and in vitro studies.

机译：在前Botzinger络合物和离子流中产生内源性节律：建模和体外研究。

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The pre-Botzinger complex is a small region in the mammalian brainstem involved in generation of the respiratory rhythm. As shown in 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-Botzinger 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-Botzinger complex andactivity of the hypoglossal (XII) nerve from in vitro transverse brainstem slices (700 micro m) of neonatal rats (P0-P4). Rhythmic activity was absent at 3 mm[K+]o but could be triggered by either the elevation of [K+]o to 5-7 mm or application of potassium current blockers (4-AP, 50-200 micro m, 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 micro m). These findings are discussed in the context of the role of endogenous bursting activity in the respiratory rhythm generation in vivo vs. in vitro and during normal breathing in vivo vs. gasping.
机译：Botzinger前体复合体是哺乳动物脑干中一个小区域，与呼吸节律的产生有关。如体外显示的，在某些条件下，该区域可以产生内源性节律性爆发活性。我们的研究集中在可能导致这种爆发行为的条件上。建立并分析了Botzinger前期复合体中起搏器神经元的计算模型。每个神经元均以霍奇金-赫克斯利（Hodgkin-Huxley）风格建模，并包括持续的钠电流和延迟整流器钾电流。我们发现，模型的点火行为在很大程度上取决于这些电流的表达。具体而言，可以通过抑制延迟整流器钾电流（直接或通过增加细胞外钾浓度[K +] o）或通过增加持续钠电流来诱导模型爆发。为了测试我们的建模预测，我们从新生大鼠的体外横脑干切片（700微米）中记录了前Botzinger复合体的内源性种群活动和舌下（XII）神经的活动。 3 mm [K +] o时没有节律性活动，但可通过将[K +] o升高至5-7 mm或应用钾电流阻滞剂（4-AP，50-200 microm或TEA，2触发）或4毫米），或通过NaCN（2毫米）阻止有氧代谢。持续的钠电流阻滞剂利鲁唑（25或50微米）可以消除这种节律性活动。在体内与体外以及体内正常呼吸与喘气之间，内源性爆发活动在呼吸节律产生中的作用中讨论了这些发现。

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