...
首页> 外文期刊>The Cerebellum >STD-Dependent and Independent Encoding of Input Irregularity as Spike Rate in a Computational Model of a Cerebellar Nucleus Neuron
【24h】

STD-Dependent and Independent Encoding of Input Irregularity as Spike Rate in a Computational Model of a Cerebellar Nucleus Neuron

机译:小脑核神经元计算模型中输入不规则性的STD依赖性和独立编码作为加标率

获取原文
获取原文并翻译 | 示例
           

摘要

Neurons in the cerebellar nuclei (CN) receive inhibitory inputs from Purkinje cells in the cerebellar cortex and provide the major output from the cerebellum, but their computational function is not well understood. It has recently been shown that the spike activity of Purkinje cells is more regular than previously assumed and that this regularity can affect motor behaviour. We use a conductance-based model of a CN neuron to study the effect of the regularity of Purkinje cell spiking on CN neuron activity. We find that increasing the irregularity of Purkinje cell activity accelerates the CN neuron spike rate and that the mechanism of this recoding of input irregularity as output spike rate depends on the number of Purkinje cells converging onto a CN neuron. For high convergence ratios, the irregularity induced spike rate acceleration depends on short-term depression (STD) at the Purkinje cell synapses. At low convergence ratios, or for synchronised Purkinje cell input, the firing rate increase is independent of STD. The transformation of input irregularity into output spike rate occurs in response to artificial input spike trains as well as to spike trains recorded from Purkinje cells in tottering mice, which show highly irregular spiking patterns. Our results suggest that STD may contribute to the accelerated CN spike rate in tottering mice and they raise the possibility that the deficits in motor control in these mutants partly result as a pathological consequence of this natural form of plasticity.
机译:小脑核(CN)中的神经元从小脑皮层的Purkinje细胞接收抑制性输入,并提供小脑的主要输出,但是它们的计算功能尚未广为人知。最近显示,浦肯野细胞的刺突活性比以前假定的更规则,并且这种规律性会影响运动行为。我们使用基于电导的CN神经元模型来研究Purkinje细胞刺的规律性对CN神经元活性的影响。我们发现增加浦肯野细胞活动的不规则性会加速CN神经元的尖峰频率,并且这种输入不规则性的重新编码机制作为输出尖峰率取决于会聚到CN神经元上的浦肯野细胞的数量。对于高收敛比率,由不规则性引起的尖峰速率加速取决于Purkinje细胞突触处的短期抑制(STD)。在低收敛比率下,或对于同步的Purkinje单元输入,发射速率的增加与STD无关。输入不规则向输出峰值速率的转化是响应于人工输入峰值序列以及从在蹒跚学步的老鼠中从Purkinje细胞记录的峰值序列而发生的,这显示出高度不规则的峰值模式。我们的结果表明,STD可能有助于蹒跚小鼠的CN尖峰速率加快,并且它们增加了这些突变体中运动控制缺陷的部分可能是这种自然形式的可塑性造成的病理结果的可能性。

著录项

  • 来源
    《The Cerebellum》 |2011年第4期|667-682|共16页
  • 作者单位

    Science and Technology Research Institute University of Hertfordshire College Lane Hatfield AL10 9AB UK;

    Department of Neuroscience Erasmus MC Dr Molewaterplein 40 3015 GD Rotterdam The Netherlands;

    Science and Technology Research Institute University of Hertfordshire College Lane Hatfield AL10 9AB UK;

    Science and Technology Research Institute University of Hertfordshire College Lane Hatfield AL10 9AB UK;

    Science and Technology Research Institute University of Hertfordshire College Lane Hatfield AL10 9AB UK;

    Department of Neuroscience Erasmus MC Dr Molewaterplein 40 3015 GD Rotterdam The Netherlands;

    Science and Technology Research Institute University of Hertfordshire College Lane Hatfield AL10 9AB UK;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    Cerebellar nuclei; Purkinje cell; Short-term depression; Tottering; Ataxia;

    机译:小脑核;浦肯野细胞;短期抑郁;蹒跚;共济失调;

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号