We formulate a conductance-based model for a 3-neuron motif associated with Childhood Absence Epilepsy (CAE). The motif consists of neurons from the thalamic relay (TC) and reticular nuclei (RT) and the cortex (CT). We focus on a genetic defect common to the mouse homolog of CAE which is associated with loss of GABA_A receptors on the TC neuron, and the fact that myelination of axons as children age can increase the conduction velocity between neurons. We show the combination of low GABA_A mediated inhibition of TC neurons and the long corticothalamic loop delay gives rise to a variety of complex dynamics in the motif, including bistability. This bistability disappears as the corticothalamic conduction delay shortens even though GABA_A activity remains impaired. Thus the combination of deficient GABA_A activity and changing axonal myelination in the corticothalamic loop may be sufficient to account for the clinical course of CAE.

中文翻译：

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儿童缺席性癫痫发作数量增加：时间延迟和双稳态。

我们为与儿童缺席癫痫症（CAE）相关的3-神经元基序制定了基于电导的模型。母题由来自丘脑中继（TC）和网状核（RT）和皮质（CT）的神经元组成。我们关注与CAE小鼠同源物常见的遗传缺陷，该缺陷与TC神经元上GABA _A受体的丢失有关，而随着儿童年龄的增长，轴突的髓鞘化可以增加神经元之间的传导速度。我们显示了低GABA _A介导的TC神经元抑制作用和长皮质丘脑回路延迟的组合，引起了多种复杂的动态变化，包括双稳态。即使GABA _A，双稳态也随着皮质丘脑传导延迟的缩短而消失_。活动仍然受到损害。因此，不足的GABA _A活性和皮质丘脑回路中轴突髓鞘改变的结合可能足以说明CAE的临床过程。