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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Calcium-activated nonspecific cation current and synaptic depression promote network-dependent burst oscillations
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Calcium-activated nonspecific cation current and synaptic depression promote network-dependent burst oscillations

机译：钙激活的非特异性阳离子电流和突触抑制促进依赖网络的猝发振荡

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摘要

Central pattern generators (CPGs) produce neural-motor rhythms that often depend on specialized cellular or synaptic properties such as pacemaker neurons or alternating phases of synaptic inhibition. Motivated by experimental evidence suggesting that activity in the mammalian respiratory CPG, the preBoetzinger complex, does not require either of these components, we present and analyze a mathematical model demonstrating an unconventional mechanism of rhythm generation in which glutamatergic synapses and the short-term depression of excitatory transmission play key rhythmo-genic roles. Recurrent synaptic excitation triggers postsynaptic Ca~(2+)-activated nonspecific cation current (I_(CAN)) to initiate a network-wide burst. Robust depolarization due to I_(CAN) also causes voltage-dependent spike inactivation, which diminishes recurrent excitation and thus attenuates postsynaptic Ca~(2+) accumulation. Consequently, activity-dependent outward currents-produced by Na/K ATPase pumps or other ionic mechanisms-can terminate the burst and cause a transient quiescent state in the network. The recovery of sporadic spiking activity rekindles excitatory interactions and initiates a new cycle. Because synaptic inputs gate postsynaptic burst-generating conductances, this rhythm-generating mechanism represents a new paradigm that can be dubbed a 'group pacemaker' in which the basic rhythmogenic unit encompasses a fully interdependent ensemble erf synaptic and intrinsic components. This conceptual framework should be considered as an alternative to traditional models when analyzing CPGs for which mechanistic details have not yet been elucidated.
机译：中央模式发生器（CPG）产生的神经运动节律通常取决于特定的细胞或突触特性，例如起搏器神经元或突触抑制的交替阶段。受实验证据提示，在哺乳动物呼吸CPG（preBoetzinger复合体）中的活性不需要这些成分中的任何一种，我们提出并分析了一个数学模型，该模型证明了非常规的节律产生机理，其中谷氨酸能突触和短期抑郁症兴奋性传递起着重要的节律性作用。复发性突触激发触发突触后Ca〜（2+）激活的非特异性阳离子电流（I_（CAN）），以启动网络范围的猝发。由于I_（CAN）而引起的强力去极化也会引起电压依赖性的尖峰失活，从而减少了反复激发，从而减弱了突触后Ca〜（2+）的积累。因此，由Na / K ATPase泵或其他离子机制产生的依赖于活动的外向电流可以终止猝发并在网络中引起瞬态静态。零星尖峰活动的恢复重新激发了兴奋性相互作用，并启动了一个新的周期。因为突触输入控制突触后爆发的电导，所以这种节奏产生机制代表了一种新的范式，可以称为“组起搏器”，其中基本的节奏产生单元包含一个完全相互依赖的合奏的erf突触和内在成分。在分析尚未阐明其机械细节的CPG时，应考虑使用此概念框架替代传统模型。

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    Jonathan E. Rubin; John .A. Hayes; Jeffrey L Mendenhall; Christopher A. Del Negro;

  • 作者单位

    Department of Mathematics, 301 Thackeray Hall, University of Pittsburgh, Pittsburgh, PA 15260;

    Department of Applied Science, 318 McGlothlin-Street Hall, The College of William and Mary, Williamsburg, VA 23187-8795 Department of Biology, Integrated Science Center 1, The College of William and Mary, Williamsburg, VA 23187-8795;

    Department of Applied Science, 318 McGlothlin-Street Hall, The College of William and Mary, Williamsburg, VA 23187-8795;

    Department of Applied Science, 318 McGlothlin-Street Hall, The College of William and Mary, Williamsburg, VA 23187-8795;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
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  • 关键词

    breathing; burst mechanism; central pattern generator;

    机译：呼吸;爆发机制中央模式发生器;

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