• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Computational Neuroscience >Biophysical mechanism of spike threshold dependence on the rate of rise of the membrane potential by sodium channel inactivation or subthreshold axonal potassium current
【24h】

Biophysical mechanism of spike threshold dependence on the rate of rise of the membrane potential by sodium channel inactivation or subthreshold axonal potassium current

机译：尖峰阈值依赖于钠通道失活或亚阈值轴突钾电流引起的膜电位升高速率的生物物理机制

获取原文
获取原文并翻译 | 示例
       
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Spike threshold filters incoming inputs and thus gates activity flow through neuronal networks. Threshold is variable, and in many types of neurons there is a relationship between the threshold voltage and the rate of rise of the membrane potential (dVm/dt) leading to the spike. In primary sensory cortex this relationship enhances the sensitivity of neurons to a particular stimulus feature. While Na~+ channel inactivation may contribute to this relationship, recent evidence indicates that K~+ currents located in the spike initiation zone are crucial. Here we used a simple Hodgkin-Huxley biophysical model to systematically investigate the role of K~+ and Na~+ current parameters (activation voltages and kinetics) in regulating spike threshold as a function of dVm/dt. Threshold was determined empirically and not estimated from the shape of the Vm prior to a spike. This allowed us to investigate intrinsic currents and values of gating variables at the precise voltage threshold. We found that Na~+ inactivation is sufficient to produce the relationship provided it occurs at hyperpolarized voltages combined with slow kinetics. Alternatively, hyperpolariza-tion of the K~+ current activation voltage, even in the absence of Na~+ inactivation, is also sufficient to produce the relationship. This hyperpolarized shift of K~+ activation allows an outward current prior to spike initiation to antagonize the Na~+ inward current such that it becomes self-sustaining at a more depolarized voltage. Our simulations demonstrate parameter constraints on Na~+ inactivation and the biophysical mechanism by which an outward current regulates spike threshold as a function of dVm/dt.
机译：峰值阈值过滤输入的输入，从而控制通过神经元网络的活动流。阈值是可变的，并且在许多类型的神经元中，阈值电压与导致尖峰的膜电位的上升速率（dVm / dt）之间存在关系。在初级感觉皮层中，这种关系增强了神经元对特定刺激特征的敏感性。尽管Na〜+通道失活可能与这种关系有关，但最近的证据表明，位于尖峰起始区的K〜+电流至关重要。在这里，我们使用一个简单的霍奇金-赫克斯利（Hodgkin-Huxley）生物物理模型系统地研究了K〜+和Na〜+电流参数（激活电压和动力学）在调节尖峰阈值（取决于dVm / dt）中的作用。阈值是凭经验确定的，而不是根据尖峰之前Vm的形状估算的。这使我们能够在精确的电压阈值下研究固有电流和门控变量的值。我们发现，Na〜+失活足以产生这种关系，只要它在超极化电压下结合缓慢的动力学发生。另外，即使没有Na +失活，K +电流激活电压的超极化也足以产生这种关系。 K +激活的这种超极化移动允许在尖峰开始之前有一个向外的电流拮抗Na +的向内电流，从而使其在更去极化的电压下变得自持。我们的模拟表明了Na〜+失活和生物物理机制的参数约束，通过该约束，外向电流根据dVm / dt调节尖峰阈值。

著录项

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