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刺激诱导的具有去抑制作用的丘脑皮层模型中的癫痫棘波放电。

Stimulus-induced Epileptic Spike-Wave Discharges in Thalamocortical Model with Disinhibition.

机构信息

School of Mathematics and Physics, University of Science and Technology Beijing, Beijing 100083, P. R. China.

Department of Dynamics and Control, Beihang University, Beijing 100191, P. R. China.

出版信息

Sci Rep. 2016 Nov 23;6:37703. doi: 10.1038/srep37703.

DOI:10.1038/srep37703
PMID:27876879
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5120301/
Abstract

Epileptic absence seizure characterized by the typical 2-4 Hz spike-wave discharges (SWD) are known to arise due to the physiologically abnormal interactions within the thalamocortical network. By introducing a second inhibitory neuronal population in the cortical system, here we propose a modified thalamocortical field model to mathematically describe the occurrences and transitions of SWD under the mutual functions between cortex and thalamus, as well as the disinhibitory modulations of SWD mediated by the two different inhibitory interneuronal populations. We first show that stimulation can induce the recurrent seizures of SWD in the modified model. Also, we demonstrate the existence of various types of firing states including the SWD. Moreover, we can identify the bistable parametric regions where the SWD can be both induced and terminated by stimulation perturbations applied in the background resting state. Interestingly, in the absence of stimulation disinhibitory functions between the two different interneuronal populations can also both initiate and abate the SWD, which suggests that the mechanism of disinhibition is comparable to the effect of stimulation in initiating and terminating the epileptic SWD. Hopefully, the obtained results can provide theoretical evidences in exploring dynamical mechanism of epileptic seizures.

摘要

癫痫失神发作的特征是典型的 2-4 Hz 棘慢波放电 (SWD),已知其是由于丘脑皮质网络内的生理异常相互作用引起的。通过在皮质系统中引入第二个抑制性神经元群体,我们在这里提出了一个改进的丘脑皮质场模型,以数学方式描述在皮质和丘脑之间的相互作用以及由两种不同的抑制性中间神经元群体介导的 SWD 去抑制调制下 SWD 的发生和转变。我们首先表明,刺激可以在改进的模型中诱导 SWD 的复发性发作。此外,我们还证明了存在各种类型的发射状态,包括 SWD。此外,我们可以识别双稳态参数区域,在该区域中,刺激可以在背景静息状态下施加的干扰来同时诱导和终止 SWD。有趣的是,在没有刺激的情况下,两种不同的中间神经元群体之间的去抑制功能也可以起始和终止 SWD,这表明去抑制的机制与刺激在起始和终止癫痫 SWD 中的作用相当。希望获得的结果可以为探索癫痫发作的动力学机制提供理论依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef15/5120301/8b08d7d535e6/srep37703-f15.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef15/5120301/14325bad4a16/srep37703-f9.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef15/5120301/85f64e98ca2c/srep37703-f11.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef15/5120301/8b08d7d535e6/srep37703-f15.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef15/5120301/254ec38056b8/srep37703-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef15/5120301/46cb11f50189/srep37703-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef15/5120301/90688d61a195/srep37703-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef15/5120301/24396c2ec023/srep37703-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef15/5120301/21caf589a032/srep37703-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef15/5120301/15dcb7387095/srep37703-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef15/5120301/dcb8e806e720/srep37703-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef15/5120301/f8b0c301722d/srep37703-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef15/5120301/14325bad4a16/srep37703-f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef15/5120301/476a3dd24a88/srep37703-f10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef15/5120301/85f64e98ca2c/srep37703-f11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef15/5120301/3698e62c682b/srep37703-f12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef15/5120301/80469a64718f/srep37703-f13.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef15/5120301/3256b13857f5/srep37703-f14.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef15/5120301/8b08d7d535e6/srep37703-f15.jpg

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Critical Roles of the Direct GABAergic Pallido-cortical Pathway in Controlling Absence Seizures.直接γ-氨基丁酸能苍白球-皮质通路在控制失神发作中的关键作用。
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