Absence epileptiform activities are traditionally considered to be primarily induced by abnormal interactions between the cortical and thalamic neurons, which form the thalamocortical circuit in the brain. The basal ganglia, as an organizational unit in the brain, has close input and output relationships with the thalamocortical circuit. Although several studies report that the basal ganglia may participate in controlling and regulating absence epileptiform activities, to date, there have been no studies regarding whether the basal ganglia directly cause absence epileptiform activities. In this paper, we built a basal ganglia-corticothalamic network model to determine the role of basal ganglia in this disease. We determined that absence epileptiform activities might be directly induced by abnormal coupling strengths on certain pivotal pathways in the basal ganglia. These epileptiform activities can be well controlled by the coupling strengths of three major pathways that project from the thalamocortical network to the basal ganglia. The results implied that the substantia nigra pars compacta (SNc) can be considered to be the effective treatment target area for inhibiting epileptiform activities, which supports the observations of previous studies. Particularly, as a major contribution of this paper, we determined that the final presentation position of the epileptic slow spike waves is not limited to the cerebral cortex; these waves may additionally appear in the thalamus, striatal medium spiny neurons, striatal fast spiking interneuron, the SNc, subthalamic nucleus, substantia nigra pars reticulata and globus pallidus pars externa. In addition, consistent with several previous studies, the delay in the network was observed to be a critical factor for inducing transitions between different types of absence epileptiform activities. Our new model not only explains the onset and control mechanism but also provides a unified framework to study similar problems in neuron systems.

中文翻译：

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基底节在缺乏癫痫样活动发展中的调控作用

传统上，缺乏癫痫样活动被认为主要是由皮质和丘脑神经元之间的异常相互作用引起的，它们在大脑中形成丘脑皮质回路。基底神经节作为大脑中的组织单位，与丘脑皮质回路有着密切的输入和输出关系。尽管有几项研究报告称基底神经节可能参与控制和调节失神癫痫样活动，但至今尚无关于基底神经节是否直接引起失神癫痫样活动的研究。在本文中，我们建立了基底神经节-皮层丘脑网络模型来确定基底神经节在该疾病中的作用。我们确定缺乏癫痫样活动可能直接由基底节中某些关键通路上的异常偶联强度引起。这些癫痫样活动可以通过从丘脑皮层网络投射到基底神经节的三个主要途径的耦合强度得到很好的控制。结果暗示黑质致密部（SNc）可以被认为是抑制癫痫样活动的有效治疗目标区域，这支持了先前研究的观察结果。特别是，作为本文的主要贡献，我们确定了癫痫慢尖峰波的最终表现位置不限于大脑皮层；而是在大脑皮层中。这些波可能还会出现在丘脑，纹状体中棘神经元，纹状体快速突触中间神经元，SNc，丘脑下核，黑质和网状苍白球。另外，与先前的一些研究一致，观察到网络延迟是诱导不同类型的缺乏癫痫样活动之间转变的关键因素。我们的新模型不仅解释了发作和控制机制，还提供了一个统一的框架来研究神经元系统中的类似问题。