Basal ganglia (BG) has been demonstrated to play the role of modulation for absence seizure generated in the corticothalamic (CT) circuit. But it is unknown what the principle of modulation is and how to improve the modulation if BG fails to hold back the absence seizures. Although neurostimulation has been surgically employed to improve the clinical symptom of patients with epilepsy, the mechanism underlying the neurostimulation regulation is still unclear. In addition, it is not clear what sort of the spatiotemporal patterned stimulation protocols can effectively abate absence seizures with less side effect and energy consumption. Here, we address these issues on the previously proposed BG-CT model. In particular, we develop a reduced corticothalamic (RCT) moldel by viewing BG as a 2I:3O feedback modulator. By calculating the mean firing rate (MFR) and triggering mean firing rate (TMFR), we find that absence seizures can be induced or abated using the neurostimulations through driving the MFRs of the related neurons to fall into or be kicked out of the regions bounded by the TMFRs. In particular, closed-loop m: n ON-OFF anodic-cathodic-cathodic (ACC) triphase coordinated resetting stimulation (CRS) applied on the CT circuit and designed with the TMFR of subthalamic nucleus (STN) in BG could achieve the satisfying abatement effects of absence seizures with the least current consumption.

中文翻译：

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基底神经节向皮质丘脑回路的反馈调制激发的无癫痫发作的闭环控制。

基底神经节（BG）已被证明发挥了在皮质丘脑（CT）回路中产生的失神发作的调节作用。但尚不清楚调制的原理是什么，以及如果BG无法阻止缺席发作，如何改善调制。尽管神经刺激已被外科手术用于改善癫痫患者的临床症状，但是神经刺激调节的基本机制仍不清楚。此外，尚不清楚哪种时空模式刺激方案可以有效减轻无神志发作，且副作用和能量消耗更少。在这里，我们通过先前提出的BG-CT模型解决这些问题。特别是，我们通过将BG视为2I：3O反馈调制器，开发了一种还原型皮质醇（RCT）模具。通过计算平均放电率（MFR）和触发平均放电率（TMFR），我们发现可以通过驱动相关神经元的MFR落入或踢出边界区域，使用神经刺激来诱发或减轻失神发作。通过TMFR。特别是，将闭环m：n开-关阳极-阴极-阴极（ACC）三相协调复位刺激（CRS）应用于CT电路，并用BG的丘脑下丘脑核（STN）的TMFR进行设计，可以实现令人满意的减排效果电流消耗最少的癫痫发作的影响。