Centre for Robotics and Neural Systems, School of Computing and Mathematics, The University of Plymouth Plymouth, UK.
Centre for Robotics and Neural Systems, School of Computing and Mathematics, The University of Plymouth Plymouth, UK ; Neural Networks Laboratory, Institute of Mathematical Problems in Biology, Russian Academy of Sciences Pushchino, Russia.
Front Comput Neurosci. 2013 Dec 2;7:173. doi: 10.3389/fncom.2013.00173. eCollection 2013.
Experiments in rodent models of Parkinson's disease have demonstrated a prominent increase of oscillatory firing patterns in neurons within the Parkinsonian globus pallidus (GP) which may underlie some of the motor symptoms of the disease. There are two main pathways from the cortex to GP: via the striatum and via the subthalamic nucleus (STN), but it is not known how these inputs sculpt the pathological pallidal firing patterns. To study this we developed a novel neural network model of conductance-based spiking pallidal neurons with cortex-modulated input from STN neurons. Our results support the hypothesis that entrainment occurs primarily via the subthalamic pathway. We find that as a result of the interplay between excitatory input from the STN and mutual inhibitory coupling between GP neurons, a homogeneous population of GP neurons demonstrates a self-organizing dynamical behavior where two groups of neurons emerge: one spiking in-phase with the cortical rhythm and the other in anti-phase. This finding mirrors what is seen in recordings from the GP of rodents that have had Parkinsonism induced via brain lesions. Our model also includes downregulation of Hyperpolarization-activated Cyclic Nucleotide-gated (HCN) channels in response to burst firing of GP neurons, since this has been suggested as a possible mechanism for the emergence of Parkinsonian activity. We found that the downregulation of HCN channels provides even better correspondence with experimental data but that it is not essential in order for the two groups of oscillatory neurons to appear. We discuss how the influence of inhibitory striatal input will strengthen our results.
帕金森病啮齿动物模型实验表明,帕金森病苍白球(GP)内神经元的振荡放电模式明显增加,这可能是该疾病一些运动症状的基础。从皮层到 GP 有两条主要途径:通过纹状体和通过丘脑底核(STN),但尚不清楚这些输入如何塑造病理性苍白球放电模式。为了研究这一点,我们开发了一种基于电流的尖峰 GP 神经元的新型神经网络模型,具有来自 STN 神经元的皮层调节输入。我们的结果支持了以下假设:同步主要通过丘脑底核途径发生。我们发现,由于来自 STN 的兴奋性输入和 GP 神经元之间的相互抑制耦合之间的相互作用,一组同质的 GP 神经元表现出自我组织的动态行为,其中两组神经元出现:一组与皮层节律同相,另一组反相。这一发现反映了在通过脑损伤诱导帕金森病的啮齿动物 GP 记录中观察到的情况。我们的模型还包括对 GP 神经元爆发放电的 Hyperpolarization-activated Cyclic Nucleotide-gated (HCN) 通道的下调,因为这被认为是帕金森活动出现的一种可能机制。我们发现,HCN 通道的下调与实验数据的吻合更好,但对于两组振荡神经元的出现并非必不可少。我们讨论了抑制性纹状体输入的影响将如何增强我们的结果。