Neuroplasticity in respiratory motor control.
Neuroplasticity in respiratory motor control.
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DOI：
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发表时间：
2003
影响因子：
3.3
通讯作者：
G. Mitchell;Stephen M. Johnson
中科院分区：
文献类型：
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作者：
G. Mitchell;Stephen M. Johnson
尽管最近的证据表明呼吸控制系统具有相当大的神经可塑性，但缺乏一个全面的概念框架。我们在这篇综述中的目标是定义与呼吸控制有关的可塑性(和相关的神经特性)，并讨论呼吸可塑性的潜在部位、机制和已知类别。呼吸可塑性被定义为神经控制系统基于先前经验的持续变化。可塑性可能涉及结构和/或功能的改变(最常见的是两者兼而有之)，并且可以由呼吸控制系统中不同部位的多种细胞/突触机制引起。呼吸神经可塑性在很大程度上依赖于必要前提条件的建立、刺激模式、对立调节系统、年龄、性别和遗传学之间的平衡。呼吸可塑性可由低氧、高碳酸血症、运动、损伤、应激和药物干预或条件作用诱导，发生在发育过程中以及成年人身上。发育可塑性是由敏感发育时期的经历(例如，改变呼吸气体)诱导的，从而改变了成熟的呼吸控制。在以后的生活中，同样的经历几乎没有效果。在成人中，神经调节在几种形式的呼吸可塑性中起着突出的作用。例如，5-羟色胺能调节被认为在间歇性低氧、反复高碳酸血症运动、脊髓感觉丧失、脊髓损伤以及至少一些条件反射后启动和/或维持呼吸可塑性。在我们充分了解呼吸可塑性的生物学意义、其潜在的细胞/分子和网络机制以及利用呼吸可塑性作为治疗工具的潜力之前，有必要进行大量的工作。
Although recent evidence demonstrates considerable neuroplasticity in the respiratory control system, a comprehensive conceptual framework is lacking. Our goals in this review are to define plasticity (and related neural properties) as it pertains to respiratory control and to discuss potential sites, mechanisms, and known categories of respiratory plasticity. Respiratory plasticity is defined as a persistent change in the neural control system based on prior experience. Plasticity may involve structural and/or functional alterations (most commonly both) and can arise from multiple cellular/synaptic mechanisms at different sites in the respiratory control system. Respiratory neuroplasticity is critically dependent on the establishment of necessary preconditions, the stimulus paradigm, the balance between opposing modulatory systems, age, gender, and genetics. Respiratory plasticity can be induced by hypoxia, hypercapnia, exercise, injury, stress, and pharmacological interventions or conditioning and occurs during development as well as in adults. Developmental plasticity is induced by experiences (e.g., altered respiratory gases) during sensitive developmental periods, thereby altering mature respiratory control. The same experience later in life has little or no effect. In adults, neuromodulation plays a prominent role in several forms of respiratory plasticity. For example, serotonergic modulation is thought to initiate and/or maintain respiratory plasticity following intermittent hypoxia, repeated hypercapnic exercise, spinal sensory denervation, spinal cord injury, and at least some conditioned reflexes. Considerable work is necessary before we fully appreciate the biological significance of respiratory plasticity, its underlying cellular/molecular and network mechanisms, and the potential to harness respiratory plasticity as a therapeutic tool.