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首页> 外文期刊>Journal of Computational Neuroscience >Reciprocal inhibition and slow calcium decay in perigeniculate interneurons explain changes of spontaneous firing of thalamic cells caused by cortical inactivation
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Reciprocal inhibition and slow calcium decay in perigeniculate interneurons explain changes of spontaneous firing of thalamic cells caused by cortical inactivation

机译：周生中间神经元的相互抑制和缓慢的钙衰减解释了皮质失活引起的丘脑细胞自发放电的变化

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The role of cortical feedback in the thalamocortical processing loop has been extensively investigated over the last decades. With an exception of several cases, these searches focused on the cortical feedback exerted onto thalamo-cortical relay (TC) cells of the dorsal lateral geniculate nucleus (LGN). In a previous, physiological study, we showed in the cat visual system that cessation of cortical input, despite decrease of spontaneous activity of TC cells, increased spontaneous firing of their recurrent inhibitory interneurons located in the perigeniculate nucleus (PGN). To identify mechanisms underlying such functional changes we conducted a modeling study in NEURON on several networks of point neurons with varied model parameters, such as membrane properties, synaptic weights and axonal delays. We considered six network topologies of the retino-geniculo-cortical system. All models were robust against changes of axonal delays except for the delay between the LGN feed-forward interneuron and the TC cell. The best representation of physiological results was obtained with models containing reciprocally connected PGN cells driven by the cortex and with relatively slow decay of intracellular calcium. This strongly indicates that the thalamic reticular nucleus plays an essential role in the cortical influence over thalamo-cortical relay cells while the thalamic feed-forward interneurons are not essential in this process. Further, we suggest that the dependence of the activity of PGN cells on the rate of calcium removal can be one of the key factors determining individual cell response to elimination of cortical input.
机译：在过去的几十年中，对皮质反馈在丘脑皮质处理环路中的作用进行了广泛研究。除少数情况外，这些搜索的重点是施加在背外侧膝状核（LGN）的丘脑皮质中继（TC）细胞上的皮质反馈。在先前的生理研究中，我们在猫视觉系统中显示，尽管TC细胞的自发活动减少，皮质输入的停止也会增加其位于周生核（PGN）的抑制性中间神经元的自发放电。为了确定这种功能改变的潜在机制，我们在NEURON中对具有不同模型参数（例如膜特性，突触权重和轴突延迟）的多个点神经元网络进行了建模研究。我们考虑了视网膜-基因-皮层系统的六种网络拓扑。除了LGN前馈中间神经元和TC细胞之间的延迟，所有模型均能抵抗轴突延迟的变化。用包含由皮质驱动的相互连接的PGN细胞且细胞内钙的衰变相对较慢的模型可获得生理结果的最佳表示。这有力地表明，丘脑网状核在皮质对丘脑皮质中继细胞的影响中起着至关重要的作用，而丘脑前馈中间神经元在该过程中不是必需的。此外，我们建议，PGN细胞活性对钙去除速率的依赖性可能是决定单个细胞对消除皮质输入的反应的关键因素之一。

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