Hu Bing, Guo Daqing, Wang Qingyun
Department of Dynamics and Control, Beihang University, Beijing, 100191 China.
Key Laboratory for Neuro Information of Ministry of Education, School of Life Science and Technology, University of Electronic Science and Technology of China, Chengdu, 610054 China.
Cogn Neurodyn. 2015 Jun;9(3):279-89. doi: 10.1007/s11571-014-9321-1. Epub 2014 Nov 25.
The cerebral cortex, thalamus and basal ganglia together form an important network in the brain, which is closely related to several nerve diseases, such as parkinson disease, epilepsy seizure and so on. Absence seizure can be characterized by 2-4 Hz oscillatory activity, and it can be induced by abnormal interactions between the cerebral cortex and thalamus. Many experimental results have also shown that basal ganglia are a key neural structure, which closely links the corticothalamic system in the brain. Presently, we use a corticothalamic-basal ganglia model to study which pathways in corticothalamic system can induce absence seizures and how these oscillatory activities can be controlled by projections from the substantia nigra pars reticulata (SNr) to the thalamic reticular nucleus (TRN) or the specific relay nuclei (SRN) of the thalamus. By tuning the projection strength of the pathway "Excitatory pyramidal cortex-SRN", "SRN-Excitatory pyramidal cortex" and "SRN-TRN" respectively, different firing states including absence seizures can appear. This indicates that absence seizures can be induced by tuning the connection strength of the considered pathway. In addition, typical absence epilepsy seizure state "spike-and-slow wave discharges" can be controlled by adjusting the activation level of the SNr as the pathways SNr-SRN and SNr-TRN open independently or together. Our results emphasize the importance of basal ganglia in controlling absence seizures in the corticothalamic system, and can provide a potential idea for the clinical treatment.
大脑皮层、丘脑和基底神经节共同构成了大脑中的一个重要网络,该网络与多种神经疾病密切相关,如帕金森病、癫痫发作等。失神发作的特征可以是2 - 4赫兹的振荡活动,它可由大脑皮层与丘脑之间的异常相互作用诱发。许多实验结果还表明,基底神经节是一个关键的神经结构,它在大脑中紧密连接皮质丘脑系统。目前,我们使用一个皮质丘脑 - 基底神经节模型来研究皮质丘脑系统中的哪些通路可以诱发失神发作,以及这些振荡活动如何受到黑质网状部(SNr)向丘脑网状核(TRN)或丘脑的特定中继核(SRN)的投射的控制。通过分别调整“兴奋性锥体皮层 - SRN”、“SRN - 兴奋性锥体皮层”和“SRN - TRN”通路的投射强度,可出现包括失神发作在内的不同放电状态。这表明通过调整所考虑通路的连接强度可以诱发失神发作。此外,当SNr - SRN和SNr - TRN通路独立或共同开放时,通过调节SNr的激活水平,可以控制典型的失神癫痫发作状态“棘慢波放电”。我们的结果强调了基底神经节在控制皮质丘脑系统失神发作中的重要性,并可为临床治疗提供一个潜在的思路。